Dilated Central Veins Research Articles

Pretreatment administration of hydro-ethanolic extract of Syzygium aromaticum prevents thioacetamide-induced liver injury in rat

IntroductionLiver injury is an important problem in healthcare. Thioacetamide (TAA)-induced liver injury is an established model in experimental research for assessing the impact of various toxins and pharmaceuticals on the liver. TAA induces its harmful effects by the production of oxidative biomolecules. Oxidative stress subsequently alters liver function, resulting in alterations in the enzymatic activity of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP). Syzygium aromaticum has significant antioxidant and anti-inflammatory properties and has been utilised in traditional medicine for liver diseases. Therefore, this study evaluated the hepatoprotective effect of the hydro-ethanolic extract of Syzygium aromaticum (HESA) against TAA-induced liver injury.Material and methodsHepatotoxicity was induced with intraperitoneal administration of TAA (150 mg/kg body weight, 3 days per week for 4 weeks) in Wistar rats. The pretreatment with HESA was conducted at three doses of 50, 150, and 300 mg/kg body weight, administered orally, starting 4 weeks before TAA administration and continued for 8 weeks. The activities of serum AST, ALT, and ALP, as well as liver superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), and malondialdehyde (MDA), were assessed. Histopathological analyses were conducted using hematoxylin and eosin (H&E) staining.ResultsThe findings showed that HESA pretreatment significantly lowered TAA-induced oxidative stress. Additionally, TAA significantly increased AST, ALT, and ALP serum levels, whereas HESA significantly recovered the corresponding values. H&E staining also showed that TAA-induced structural liver damage was characterised by central vein dilatation, and necrosis, and apoptosis in adjacent cells. The histopathological findings of the TAA group were partially recovered in the pretreatment extract groups.ConclusionThe results of this study support the antioxidant and anti-inflammatory properties of Syzygium aromaticum against TAA-induced liver injury.

The possible protective effect of luteolin on cardiovascular and hepatic changes in metabolic syndrome rat model.

The metabolic syndrome, or MetS, is currently a global health concern. The anti-inflammatory, anti-proliferative, and antioxidant properties of luteolin are some of its advantageous pharmacological characteristics. This research was designed to establish a MetS rat model and investigate the possible protective effect of luteolin on cardiovascular, hepatic, and metabolic changes in diet-induced metabolic syndrome in rats. Forty adult male albino rats were split into four groups: a negative control group, a group treated with luteolin, a group induced MetS (fed 20% fructose), and a group treated with luteolin (fed 20% fructose and given luteolin). Following the experiment after 8weeks, biochemical, histological (light and electron), and immunohistochemistry analyses were performed on liver and heart tissues. Serum levels of cTnI, CK-MB, and LDH were significantly elevated in response to the cardiovascular effect of MetS. Furthermore, compared to the negative control group, the MetS group showed a marked increase in lipid peroxidation in the cardiac and hepatic tissues, as evidenced by elevated levels of MDA and a decline in the antioxidant defense system, as demonstrated by lower activities of GSH and SOD. The fatty liver-induced group exhibited histological alterations, including disrupted hepatic architecture, dilated and congested central veins, blood sinusoids, and portal veins. In addition to nuclear structural alterations, most hepatocytes displayed varying degrees of cytoplasmic vacuolation, mitochondrial alterations, and endoplasmic reticulum dilatation. These alterations were linked to inflammatory cellular infiltrations, collagen fiber deposition, active hepatic stellate cells, and scattered hypertrophied Kupffer cells, as demonstrated by electron microscopy and validated by immunohistochemical analysis. It is interesting to note that eosinophils were seen between the liver cells and in dilated blood sinusoids. Moreover, the biochemical (hepatic and cardiac) and histological (liver) changes were significantly less severe in luteolin-treated raton a high-fructose diet.These results suggested that luteolin protects against a type of metabolic syndrome that is produced experimentally.

Ameliorative Potential of Ginger for Mitigating Liver Damage Caused by Fluopyram in Male Albino Rats

Fluopyram is a widely used new generation broad spectrum fungicide and a variety of biochemical and histopathological alterations in the livers of albino rats. These include inflammatory cells, dilated sinusoids, haemorrhage, dilation of central veins, congestion and presence of erythrocytes. Significant increase in blood alanine aminotransferase (ALT), aspartate amino transferase (AST), acid phosphatise (ACP) and decrease in alkaline phosphatise (AKP) enzyme levels were seen in high dose of fluopyram treated rats as compared to control. The oxidative stress and antioxidant enzymes showed a significant reduction in superoxide dismutase (SOD), catalase (CAT) and increase in malondialdehyde (MDA) level. Rats treated with fluopyram and ginger showed improved histopathological changes in liver. Ginger extract also showed decreased serum levels of malondialdehyde and raised serum levels of antioxidant enzymes. According to the current study, strong antioxidant activity of ginger mediates its protective effect against fluopyram induced liver damage.

Evaluation of the healing and protective properties of adipose-derived mesenchymal stem cells from cisplatin-induced liver and kidney damage.

The occurrence of nephrotoxicity and hepatotoxicity as a result of cisplatin administration is a major concern in clinical practice. This study examined the potential protective effects of administering mesenchymal stem cells (MSCs) on the renal and hepatic damage caused by cisplatin. Moreover, the study investigated the potential protective effects of administering Adipose-Derived Mesenchymal Stem Cells (ADMSC) to counteract the harmful effects of cisplatin-induced kidney and liver damage. Male Sprague-Dawley rats were divided into three groups: normal control, cisplatin + saline, and cisplatin + ADMSC. Cisplatin was administered to induce toxicity, and ADMSC was administered intravenously as a potential therapeutic intervention. Biochemical parameters and histopathological changes were assessed in the kidney and liver tissues. Statistical analyses were performed using a one-way ANOVA. Cisplatin increased malondialdehyde (MDA), tumor necrosis factor alfa (TNF-alfa), IL-6, alanine transaminase (ALT), creatinine, Galectin-3, Tissue growth factor beta 1 (TGF-beta 1), compared to the normal control group. Cisplatin-MSC reduced these levels. Histopathology showed that cisplatin caused kidney tubular epithelial necrosis, luminal necrotic debris, tubular dilatation, interstitial inflammation, liver sinusoidal and central vein dilatation, congestion, necrosis, and cytoplasmic vacuolization. ADMSC administration significantly reduced histopathological changes. These findings highlight the potential therapeutic benefits of mesenchymal stem cell (MSC) administration in mitigating cisplatin-induced nephrotoxicity and hepatotoxicity. MSC treatment demonstrated protective effects by reducing oxidative stress, inflammatory markers, and histopathological alterations. Further investigations are warranted to elucidate the precise mechanisms underlying these protective effects and evaluate their clinical implications for managing cisplatin-induced organ damage.

Comparative impacts of Saudi Arabian and Egyptian Aspergillus flavus-associated Aflatoxin B1 on rats

Aflatoxin B1 (AFB1) is a carcinogenic secondary metabolite of filamentous Aspergillus species. This study investigated the effects of Saudi Arabian (local) and Egyptian (imported) Aspergillus flavus-associated AFB1 on rats (hematological parameters, liver, and kidneys). Saudi Arabian and Egyptian A. flavus-associated AFB1 (0.5 mg/kg) were separately fed to two groups of five rats each for 21 days. The control group (5 rats) was fed water and a basal pellet diet for 21 days (a total of 15 rats, 5 rats in each treated group and 5 rats as control). The blood samples from the rats in all the groups were subsequently examined for complete blood count (CBC) data [red blood cell (RBC), neutrophil, and platelet counts; basophil counts; eosinophil, hemoglobin (Hb) content; monocyte, lymphocyte, and mean corpuscular hemoglobin (MCH) counts; mean corpuscular volume (MCV); mean corpuscular hemoglobin concentration (MCHC); and white blood cell (WBC)]. Liver function was assessed by examining the serum levels of alkaline phosphatase (ALP), aspartate aminotransferase (AST), and albumin in all groups. The kidney function test was based on the levels of uric acid, urea, creatinine, and urea. AFB1-induced histopathological changes were observed under a light microscope. One-way ANOVA coupled with Tukey’s LSD test revealed that AFB1 in both isolates (Saudi Arabian and Egyptian) significantly decreased the RBC count, whereas a significant increase in the platelet, WBC, neutrophil, and monocyte counts was noted. Compared with the control treatment, Saudi Arabian AFB1 treatment significantly reduced the MCH and MCHC values. The serum levels of AST, ALP, urea, and creatinine were significantly greater in the Saudi Arabian AFB1-treated group than in the other two groups, whereas the level of ALB was significantly lower in this group than in the Current Research in Environmental & Applied Mycology (Journal of Fungal Biology) 14(1): 356–370 (2024) ISSN 2229-2225 www.creamjournal.org Article Doi 10.5943/cream/14/1/18 357 Egyptian AFB1-treated group and controls. Histological examination of the liver revealed central vein dilatation and congestion of the portal area with leucocyte infiltration in both AFB1-treated groups, which led to substantial cell mortality. Both AFB1 treatments caused hypertrophied hepatocytes with pyknotic nuclei and granular vacuolated cytoplasm. The AFB1-treated groups presented marked renal damage characterized by cupping of Bowman's capsule, glomerular membrane disruption, and tubular damage. However, adverse effects were more severe in the Saudi Arabian AFB1-treated group. Both AFB1 treatments induced hematological and organ toxicity in rats. However, the toxicity of Saudi Arabian A. flavus-associated AFB1 was more pronounced than that of Egyptian A. flavus-associated AFB1. The findings of the current study may help improve hygiene measures to lower mycotoxin contamination in commercial food products, as well as emphasise the health hazards posed by A. flavus-contaminated household foodstuffs.

PROTECTIVE EFFECTS OF GRAPE SEED EXTRACT (VITIS VINIFERA) AGAINST CISPLATIN-INDUCED LIVER DAMAGE IN RABBITS. (HISTOLOGICAL AND HISTOPATHOLOGICAL STUDY)

Cisplatin is a chemotherapeutic drug used in the treatment of various cancer types. It can be considered a double-edged sword. It is a potent anticancer agent at the same time has toxic effect on various tissues as it causes hepatotoxicity. It was determined to cause liver toxicity and to weaken the antioxidant defense systems in liver. A decrease in antioxidant enzymes resulted from cisplatin induced tissue toxicity. Moreover, the development of therapies to prevent the appearance of cisplatin- induced tissue toxicities has focused on administration of antioxidants along with cisplatin treatment. The grape seeds exhibit a broad spectrum of pharmacological properties against oxidative stress. Therefore, the aim of present study was designed to investigate the protective effects of grape seed extract on the liver damage in cisplatin treated rabbits. Twenty seven healthy rabbits of local mixed breed were selected, divided into three equal groups, the first group (CON group) served as control and received a single intraperitoneal injection of normal saline solution once per week for 6 weeks; the second group (CIS group) were treated with therapeutic dose of cisplatin intraperitoneally once per week for six weeks; the third group (CIS+GSE group) served as protective group and was concomitantly treated with grape seeds extract by oral gavages and cisplatin injection intraperitoneally once per week for six successive weeks. Administration of grape seeds extract by oral gavages starting from the first day of the experiment for 6 consecutive days before and 6 consecutive days after the cisplatin injection and continued daily for 6 weeks. The histopathological findings present in current study showed that cisplatin toxicity produced significant structural changes in the liver of CIS group, cisplatin treated group, in the form of prominent disorganized architecture and loss of liver lobulation, distortion of the arrangement of parenchyma of the liver, loss of radial arrangement of sinusoids from the central vein of the liver, Dilatation and congestion of central veins, sinusoids and portal traids, degenerative changes in hepatocytes and pyknotic nuclei indicating necrosis. Marked vacuolar degeneration mainly hydropic ballooning degeneration and hyper activation of Kupffer cells and inflammatory cellular infiltrations were also observed. This finding reflected the cytotoxic effects of cisplatin in hepatic tissue. While, in the sections from the liver of animals received therapeutic dose of cisplatin and treated by grape seed extract, group (CIS+GSE) clearly showed that there was a significant alleviated hepatotoxicity, since histopathological changes were markedly less pronounced compared to animals treated with cisplatin alone. Therefore, and based on our findings, the grape seed extract contributes significantly to the improvement of histological alterations in rabbit liver caused by cisplatin.

Allium sativum Essential Oil Supplementation Reverses the Hepatic Inflammation, Genotoxicity and Apoptotic Effects in Swiss Albino Mice Intoxicated with the Lead Nitrate.

Prolonged lead (Pb) exposure impairs human health due to its interference with physiological and biochemical processes. Therefore, it is necessary to investigate natural therapeutics to alleviate Pb-induced intoxication. In the current investigation, essential oil extracted from the fresh bulbs of Allium sativum was considered as a natural remedy. Initially, in vitro antioxidant and anti-inflammatory activity of A. sativum essential oil (ASEO) were explored. The results reported that ASEO exhibits potent antioxidant and anti-inflammatory potential. Additionally, an in vivo study was conducted to elucidate its preventive role against Lead-nitrate (LN)-induced hepatic damage in Swiss albino mice. The experimental mice were allocated into six groups: Control, LN-intoxicated group (50mg/kg), LN + ASEO (50mg/kg), LN + ASEO (80mg/kg), LN + Silymarin (25mg/kg), and LN + vehicle oil control group. The entire duration of the study wasof 30days. From the results, it was determined that LN exposure elevated the Pb content in hepatic tissues which subsequently increased the serum biomarkers, inflammatory cytokines (NF-kB, TNF-α, IL-6) as well as apoptotic factors (caspase-3, BAX), all of which contribute to DNA damage. Meanwhile, it reduced anti-inflammatory (IFN-γ and IL-10) and anti-apoptotic factors (Bcl-2). Furthermore, Pb accumulation in hepatic tissues changed the histological architecture, which was linked to necrosis, central vein dilation, inflammatory cell infiltration and Kupffer cell activation. In contrast to this, ASEO administration decreased the Pb content, which in turn reduced the level of serum biomarkers, inflammatory and apoptotic factors. At the same time, it increased the anti-inflammatory and anti-apoptotic factors, thereby reduced DNA damage and restored the hepatic histology. In conclusion, exhaustive research is of the utmost demand to elucidate the precise defense mechanisms of ASEO against LN-induced hepatotoxicity.

HISTOPATHOLOGICAL EFFECT OF CHLORPYRIFOS PESTICIDE ON LIVER AND KIDNEY OF FRESH WATER FISH CATLA CATLA

All the natural water bodies are continuously being contaminated with toxic chemicals from industrial, agricultural and domestic activities. Chlorpyrifos is one of the most widely used organophosphate pesticides. Excessive application of pesticides from agricultural fields contaminate aquatic medium, resulting in serious damage to non-target species, including fish. The fish as a bioindicator of aquatic medium plays an important role in the monitoring of water pollution. Histopathology is an important tool for evaluating the action of any toxicant at tissue level. The focus of the present study is to measure the histological changes in liver and kidney of the fresh water fish Catla catla exposed to sub lethal concentrations of chlorpyrifos 1/15th of the 96 hour LC50 values for the period of 10 and 20 days. The fish exposed to chlorpyrifos showed mild vacuolar hepatocytes, dilation of central vein, vaculor degenerative changes, mild hyperaemia and severe hyperaemia of central vein in the liver tissue slide. The changes observed in kidney slide due to the impact of chlorpyrifos toxicity are hemorrhage, degenerative changes in between tubules, constriction of primary tubule, vacuolardegenerative changes, necrosis in epithelial lining of proximal tubules, chlorpyrifos compound induced.

Assessing the Acute Toxicological Effects of Annona muricata Leaf Ethanol Extract on Rats: Biochemical, Histopathological, and Metabolomics Analyses.

Annona muricata is a common plant used in Africa and South America to manage various types of disease. However, there is insufficient toxicological information or published standard available regarding repeated dose animal toxicity data. As part of the safety assessment, we exposed Sprague Dawley rats to an acute oral toxicity of A. muricata. The intent of the current study was to use advanced proton nuclear magnetic resonance (1H NMR) in serum and urinary metabolomics evaluation techniques to provide the in vivo acute toxicological profile of A. muricata leaf ethanol extract in accordance with the Organization for Economic Co-operation and Development's (OECD) 423 guidelines. A single 2000 mg/kg dose of A. muricata leaf ethanol extract was administered to Sprague Dawley rats over an observational period of 14 days. The toxicity evaluation (physical and behavior observation, body weight, renal function test, liver function test and 1H NMR analysis) showed no abnormal toxicity. Histopathological analysis manifested mild changes, i.e., the treated kidney manifested mild hypercellularity of mesangial cells and mild red blood cell congestion. In addition, there was mild hemorrhage into tissue with scattered inflammatory cells and mild dilated central vein with fibrosis in the liver. However, the changes were very mild and not significant which correlate with other analyses conducted in this study (biochemical test and 1H NMR metabolomic analysis). On the other hand, urinary 1H NMR analysis collected on day 15 revealed high similarity on the metabolite variations for both untreated and treated groups. Importantly, the outcomes suggest that A. muricata leaf ethanol extract can be safely consumed at a dose of 2000 mg/kg and the LD50 must be more than 2000 mg/kg.

Effects of exposure to imidacloprid contaminated feed on the visceral organs of adult male rabbits (Oryctolagus cuniculus)

The best-known and often used systemic, broad-spectrum neonicotinoid pesticide is imidacloprid (IMI). This study was carried out on adult male rabbits (n = 12) to assess the residual effects of exposure to IMI-contaminated diet on the liver, lung, heart, and kidney. Pesticide-exposed rabbits (n = 6) received IMI contaminated green grass (Bildor® 0.5 ml (100 mg)/L water) every alternative day once daily for up to 15 days. The remaining rabbits were fed a standard diet free of pesticides as a control. During routine monitoring of the rabbits throughout the experiment, there were no apparent toxic symptoms identified. On days 16, after deep anesthesia blood and visceral organs were collected. The levels of hepatic serum aspartate transaminase and alanine transaminase were considerably elevated in IMI-exposed rabbits (p ≤ 0.05). Thin layer chromatography revealed that the residue of IMI was at the detectable level in the liver and stomach. Histopathologically, the liver revealed coagulation necrosis with granulomatous inflammation and congestion in portal areas with dilated and congested central veins. The lungs showed congestion of blood vessels and granulomatous inflammation around the terminal bronchiole. Accumulations of inflammatory cells were observed in the cortico-medullary junction in the kidney. The heart showed necrosis and infiltration of mononuclear cells within the cardiac muscles. The findings of the current study emphasize that IMI-contaminated feed exposure causes toxicity into the cellular level of different visceral organs of adult male rabbits and it may also cause the similar toxic effects of the other mammals specially the occupationally exposed persons.

TOXICITY PROFILES OF METHANOL EXTRACT OF CROSSOPTERYX FEBRIFUGA LEAF (AFZEL. EX G. DON) BENTH

Crossopteryx febrifuga is one of the plants used for the local treatment of some disease conditions by the people of Nigeria via its leaf, root and bark without knowing the toxic nature of the plant recipes. This research was designed to ascertain the toxicity profiles of the plant leaf. Acute toxicity was determined in two phases using rats. In sub-acute toxicity studies, haematology, histopathology and evaluation of liver function indices were conducted. In the first phase of the toxicity study, the mice showed no observable toxic effects as high as at 1000 mg/kg. However, it caused sluggishness, respiratory distress at higher doses in the second phase. On haematological indices, white blood cell, lymphocyte, erythrocytes, haemoglobin, haematocrit rose significantly across the doses administered. The liver function test revealed significant increase in serum alkaline phosphatase (ALP), alanine transaminase (ALT), aspartate transaminase (AST), albumin, total protein and conjugated bilirubin while 800 mg/kg extract reduced the aspartate transaminase. On histopathology, liver revealed normal hepatocytes but dilated central vein while in kidney, renal corpuscle, glomeruli and tubule were normal. On heart, revealed was active vascular congestion with normal bundle of myocardial fibres and coronary artery while in aorta, it revealed normal architecture. With the nature of the toxicity profile revealed especially at doses less than 500 mg/kg of C. febrifuga extract, the plant could be considered to be relatively safe. This study is significant as it provides information that may suggest some safe doses out of the doses used for clinical trial and application

Sub-chronic toxicity of the aqueous leaf extract of Ocimum lamiifolium Hochst. ex Benth on biochemical parameters and histopathology of liver and kidney in rats: in vivo and in- silico toxicity studies

BackgroundThe aerial part of Ocimum lamiifolium is commonly used in Ethiopian traditional medicine. Although this plant is mostly used in traditional medicine, its safety profile has not been documented yet. The aim of this study was to assess the sub-chronic toxicity of O. lamiifolium aqueous extract in rats and to determine the toxicity profile of GC–MS identified bioactive compounds obtained from essential oil of O. lamiifolium using in silico toxicity methods.MethodsEighty rats (40 male and 40 female) were randomly assigned to four groups of ten rats per sex/group. For 90 days, Groups I-III received 200, 400, and 600 mg/kg bw of aqueous extract of O. lamiifolium, respectively. Distilled water was given to Group IV (control). Clinical observations, food intake, and rat weight were all recorded during the experiment. In addition, several biochemical parameters, organ weight, and histology of the liver and kidney were all evaluated. For the in-silico toxicity study, GC–MS identified bioactive compounds in O. lamiifolium essential oil were obtained from published articles. The compounds two-dimensional structures were constructed using Chemdraw. The two-dimensional structures were converted into a simplified molecular input line entry system (SMILES) using the Swiss ADMET web tool. Furthermore, the toxicity parameters were predicted using the ProTox II server.ResultsThe administration of an aqueous extract of O. lamiifolium leaves significantly (p < 0.05) reduced the test animals' food intake and body weight gain. In the high dose (600 mg/kg bw) treated group, the serum alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase levels were significantly increased (p < 0.05). In female rats given 600 mg/kg bw of O. lamiifolium, the levels of serum urea were also increased. In addition, rats given 600 mg/kg bw had significantly lower blood glucose levels than the control group (p < 0.05). Doses up to 400 mg/kg bw didn’t bring a significant change to the histology of the liver. However, in the high dose (600 mg/kg bw) treated group, some female rats' livers showed mild sinusoidal and central vein dilatation, as well as parenchymal necrosis. our findings showed that all compounds derived from the essential oil of O. lamiifolium showed no mutagenicity or cytotoxicity. However, 30% of the compounds tested were hepatotoxic, 20% carcinogenic, and 20% immunotoxin.ConclusionOur findings showed that oral administration of O. lamiifoliums aqueous extract up to a dose of 400 mg/kg bw is not toxic. However, high-dose (600 mg/kg bw) significantly affected the food consumption and weight gain of the experimental rats and the serum concentration of some liver and kidney enzymes were also significantly increased. Additionally, a considerable proportion of the tested compounds were predicted to be hepatotoxic, carcinogenic and immunotoxin. Furthermore, before employing O. lamiifolium preparations as drugs, a chronic toxicity research on the essential oil as well as its components that exhibited toxicity in the in-silico toxicity study is needed. Finally, use high doses of O. lamiifolium leaves with caution.

Tablet Formulation with Galactomannan Binding Agent and Acute Toxicity Test from Terminalia catappa L.

Ketapang is one of the many medicinal plant species that grow in Indonesia and is used to treat various diseases. Ketapang leaves contain flavonoids, tannins, saponins, and terpenoids that have anti-inflammatory, antioxidant, antiviral, and antimicrobial properties. This study aimed to determine the LD50 and histopathology of Liver and kidney damage before the formulation of tablets containing galactomannan-binding agents. The toxicity determination method was carried out in vivo in experimental animals at doses of 4g/kg BW, 8g/kg BW and 16g/kg BW, and Liver and kidney histopathology was carried out before formulation into tablet preparations using the wet granulation method with various concentrations of binders and disintegrants, namely F1(8:0), F2(0:8), F3(4:4), F4(2:6), and F5(6:2). The results of the toxicity test showed an LD50 of 15.9959, liver damage at a dose of 4 g/kg BW hepatocyte karyorrhexis cells, central vein constriction, sinusoidal dilatation, a dose of 8 g/kg BW hepatocyte karyorrhexis, significant venous congestion, sinusoidal dilatation, a dose of 16 g/kg BW hepatocyte cells, karyolysis, dilated central veins, and dilated sinusoids. The results of the tablet mass preformulation test meet the requirements: the flow time test was 1.48-2.14 g/second, the angle of repose test was 24.60°-30.60°, and the tab index test was 5.33%-9.33%. The results of the tablet evaluation test were as follows: the tablet hardness test was 3.8-8.6 kg, the tablet friability test was 0.167-0.64%, and the tablet disintegration time test was 29.06-107.51 minutes.

Mitochondrial Homeostasis and Mast Cells in Experimental Hepatic Ischemia-Reperfusion Injury of Rats.

Background:Ischemia-reperfusion injury is a histopathological event and is an important cause of morbidity and mortality after hepatobiliary surgery. We aimed to investigate the protective effect of uridine on hepatic ischemia-reperfusion injury in rats.Methods:he animals were divided into 4 groups (n = 8): group I (control), group II: ischemia-reperfusion (30 minutes ischemia and 120 minutes reperfusion), group III: ischemia-reperfusion + uridine (at the beginning of reperfusion), and group IV: ischemia-reperfusion + uridine (5 minutes before ischemia-reperfusion). Uridine was administered a single dose of 30 mg/kg IV. The 3 elements of the hepatoduodenal ligament (hepatic artery, portal vein, and biliary tract) were obliterated for 30 minutes. Then hepatic reperfusion was achieved for 120 minutes.Results:In the ischemia-reperfusion group, both liver tissues and serum chymase activity and high-temperature requirement A2 levels were higher. Severe central vein dilatation and congestion, widening sinusoidal range, diffuse necrotic hepatocytes and dense erythrocyte accumulation in sinusoids, and strongly inducible nitric oxide synthase expression were seen in the ischemia-reperfusion group. A clear improvement was seen in both uridine co-administration and pretreatment groups.Conclusion:Our results revealed that uridine limits the development of liver damage under conditions of ischemia-reperfusion, thus contributing to an increase in hepatocyte viability.

Histopathological study on the protective effect of vitamin C against paracetamol-induced acute hepatic damage in rat.

Paracetamol (PCM) as analgesic drugs makes hepatotoxicity damage. Vitamin C (VC) has been recognized as an antioxidant and has shown protective effects against hepatotoxicity damage caused by paracetamol. The current investigation aims to study the possible protective effects of VC against hepatic damage induced by PCM in rats. Forty male rats were divided into five groups: The primary group as control; receiving distilled water orally, the second group; receiving 500 mg/kg of VC. The third group; receiving 500 mg/kg of PCM. The fourth group (protective group); receiving VC for 7 days, and then PCM for another 7 days, and the last group treated with a combination of VC and PCM for 14 days. The liver tissues after administration of PCM alone showed different changes such as disrupted lobular architecture with degenerating hepatocytes, dilated congested central vein, and mononuclear cellular infiltration. While the protective group preserved the general architecture and lacked evidence of major morphological. Additionally, VC with PCM showed some alterations in the liver architecture. In conclusion, the results of this study demonstrate that VC was effective in reducing the hepatic damage caused by PCM in male albino rats.

Histological and Biochemical Investigation of Hepato-protective Role of Vitamin B12 in Male Wistar Rats Intoxicated by Diazinon

In order to estimate the hepato-protective activity of Vit.B12 in diazinon hepatotoxic effect, the current study was performed on twenty-four male adult Wistar rats. They’d divided into four equal groups for 30 days: group A (control group) served as control; group B (Dzn group) administered an oral daily dose of 1/10 LD50 (3.8mg/ kg.bw) from diazinon; group C (Dzn + Vit.B12 group) administered an oral daily dose of 1/10 LD50 (3.8 mg / kg bw) from diazinon, in addition to the systemic intramuscular doses of (4 mg/kg) from Vit.B12 in daily basis; group D (Vit.B12 group) administered daily systemic intramuscular doses of (4 mg/kg) Vit.B12 only. The results showed that group C had a significant improvement in the antioxidant indicators compared with group B in which the CAT, GSH, and SOD serum activities showed significant increasing (P≤0.05) in group C, in addition, it revealed a significant decreasing (P≤0.05) in the values of MDA and peroxynitrite comparing to the same levels of the group B. The histological results of the liver of group C showed a great improvement compared with group B which showed normal hepatic architecture consisting of normal hepatocytes, and normal sinusoids with normal other hepatic components except mild central vein dilation. The current study concludes that vitamin B12 helps to ameliorate the diazinon hepatotoxic effects as a model for a wide spread of organophosphorus compounds in agriculture and veterinary sectors by ameliorating its harmful oxidation on the liver since vitamin B12 is cheap and available as a commercial supplement therefore we recommend its uses

Lipid Lowering and Hepatoprotective Activity of Premna Tomentosa Leaf Extract (EPT) against Alcohol Induced Toxicity in Rats

The present study aims to determine the hepatoprotective and lipid lowering property of ethanolic leaf extract of Premna tomentosa (EPT) in alcohol induced hepatotoxicity. Chronic ethanol consumption is a significant danger factor in deciding liver disorders and other metabolic conditions through various mechanisms, including the regulation of the lipid metabolism. Medicinal plants are accepted to be a significant wellspring of new chemical substances with expected remedial impacts. Premna tomentosa (Verbenaceae) is a popular medicinal plant used extensively for the treatment of various ailments widely used in liver disorders. In the present research study, the male albino Wister rats were grouped (I-V) each consisting of 6 animals. In-vivo administration of 40 % ethanol (1 ml/100 gm b w/day) for 60 days resulted in a significant elevation in Total cholesterol, Triglycerides, LDL, and VLDL levels whereas the levels of HDL was found to be decreased when compared with the control rats. Liver tissues disclose central vein and sinusoidal capillary dilation, interface hepatitis, cytoplasmic vacuolization and mononuclear cell infiltration which confirms the intensity of liver damage due to chronic alcohol ingestion. Simultaneous EPT supplementation (500mg/kg and 750 mg/kg bw) to alcohol -intoxicated rats, reduced the levels of Total cholesterol, triglycerides, and lipoproteins consequential as analogized with the unsupplemented alcohol- treated rats. Liver of rats pre-treated with ethanolic extract of Premna tomentosa (500 mg and 750 mg) manifest reduced formation of interface hepatitis, vascular congestion, and fatty degeneration and exhibits more hepatoprotection compared with the rats pre-treated in Liv 52. The blood parameters were amplified by the histopathological perusal of the liver. The lipid -lowering property by the derivatives of cinnamic acid showed anticholesteremic activity. The results confirm the Hepatoprotective and lipid -lowering ability of Premna tomentosa in alcohol-treated rats.

Pathomorphological changes in German boxer dog infected with Babesia canis parasites. Clinical case

The article covers the results of a comprehensive pathomorphological study of Babesia canis parasitic infestation in a dog of the German boxer breed. In April 2020, a male German boxer with pronounced clinical signs of anorexia, remitting fever, hematuria, and manifestations of general jaundice was admitted to the Dr. Markevych clinic (Lviv). The anamnesis evidenced that after daily walks in the park of Lychakiv district (Lviv) the pet’s owner had been detecting 3–5 Ixodes ticks on the dog’s body for several days in a row. Cytological examination of blood smears stained by the Romanovsky–Giemsa method revealed a massive lesion of erythrocytes by the Babesia canis parasite. The applied treatment strategy, namely the introduction of the drug with the active substance imidocarb dipropionate, was not successful. The dog died in the clinic. An autopsy was performed in agreement with the pet owner. Macroscopic examination revealed foamy fluid in the trachea, pulmonary edema and lobar pneumonia, massive diffuse hemorrhages on the epicardium and costal pleura, splenomegaly, serous lymphadenitis, acute venous stasis, hepatic and renal dystrophy, and pancreonecrosis. General anemia and transudate accumulation in serous cavities were established. Tissue fragments of lungs, kidneys, liver, spleen, and pancreas were selected for a histopathological examination and fixed in 10 % neutral aqueous formalin solution, followed by dehydration in alcohols, filling into paraffin blocks and subsequent production of histopreparations. Staining was performed with eosin and Ehrlich’s hematoxylin according to the conventional methods. Microscopically, the lungs showed the alveoli swelling, thickening of the alveoli walls with blood overflow, bronchioles’ inflammatory infiltration with the accumulation of desquamated epithelium and exudate in the lumens of large bronchi. Extracapillary glomerulonephritis and hyaline-drop renal tubular dystrophy were observed in the kidneys. Vascular endothelium edema, granular hepatocyte dystrophy, sharp dilation of central vein and intraparticle and interparticle capillaries were found in the liver. Significant hyperplasia was observed in the red pulp of the spleen. Reticuloendothelial proliferation, erythrocyte proliferation with a diffuse accumulation of hemosiderophages due to increased erythrocyte disintegration, sinus dilatation, and atrophy of white pulp lymph nodes were also revealed.

The Effect of Cigarette Smoke Exposure on Histology Liver in Male Mice

When smoking Reactive Oxygen Species (ROS), which is a reactive oxidizing agent, can cause damage to the DNA structure of liver cells and increase the occurrence of liver necrosis. The research aims to determine the histopathological picture of the liver in male mice (Mus musculus) exposed to cigarette smoke. This research is an experimental laboratory with the sample used is male mice (Mus musculus). The sample with the most damage in treatment I obtained 5 (55.6%) samples with a score of 2 who had damage to hepatocytes. , 7 (77.8%) samples with a score of 3 had central venous dilation, 3 (33.3%) samples with a score of 1 had fatty liver, and 3 (33.3%) samples with a score of 1 had liver necrosis. While in treatment II, 5 (55.6%) samples with a score of 2 had hepatocyte cell damage, 8 (88.9%) samples with a score of 3 had central vein dilation, 5 (55.6%) samples with a score of 3 had fatty liver, and 5 (55.6%) samples with a score of 2 had liver necrosis. Based on these results, the histopathological changes in the liver of male mice (Mus musculus) were exposed to cigarette smoke.

Evaluation of Nano-curcumin effects against Tartrazine-induced abnormalities in liver and kidney histology and other biochemical parameters.

In the current study, 40 albino male rats were investigated to evaluate the impact of Nano‐curcumin (Nano‐CUR) administration against Tartrazine (TZ)‐induced variations in kidney and liver histology and their related functions. The liver function biomarkers are (glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma‐glutamyl transaminase (GGT), alkaline phosphatase (ALP), total bilirubin (T. BiLL)), whereas the kidney biomarkers are (creatinine, uric acid, urea, globulin, total protein (TP)), as well as blood parameters of (serum glucose (sGlu), alpha‐fetoprotein (AFP), protein Kinase‐C (PKC)) and lipid profiles that include (total lipids (TL), triglyceride (TG), total cholesterol (TC), low‐density lipoprotein‐cholesterol (LDL‐C), high‐density L‐C (HDL‐C), and very‐low‐density L‐C (VLDL‐C)). The collected rats were randomly separated into four different groups (G1, G2, G3, and G4) of 10 rats each, where G1 stands for control, G2 for TZ‐ingestion, G3 for Nano‐CUR‐ingestion, and G4 for (TZ + Nano‐CUR mix.) ingestion. TZ‐ingestion significantly (p < .05) increases the liver function enzymes’ activity, total bilirubin and kidney biomarkers (creatinine, urea, uric acid, total protein (TP), globulin (Glu)). Also, TZ‐ingestion significantly increased sGlu, PKC, AFP, as well as lipid profiles, while there were significant (p < .05) decreases in HDL‐C and albumin (Alb) concentrations compared to control. Histopathological changes in liver, such as dilatation of blood sinusoids and central vein with hemorrhage and necrosis, were observed due to TZ‐ingestion. Similarly, TZ‐ingestion influenced kidney tissues in terms of tubular dilatation with tubular degeneration, thickened basement membrane, and dilatation of the glomerular capillaries. Markedly, the administration of Nano‐CUR significantly decreased liver and kidney function enzymes as well as sGlu, AFP, and PKC, whereas it significantly increased serum Alb and HDL‐C levels compared to control and TZ‐ingested rats. All values arranged around normal control values. Also, the liver tissue of Nano‐CUR‐ingested rats showed a normal arrangement of normal blood sinusoids(s), hepatic cords, and hepatocytes as compared to controls. The same results were also found in the section of rat kidney ingested with 2.00 g of Nano‐CUR/(kg B.W.) showing near‐normal architecture as compared to control rats. The liver tissue of rats ingested by a mixture of (7.5 mg of TZ + 2.0 g of Nano‐CUR/kg B.W.) showed little necrosis. Similarly, a section of rat kidney ingested a mixture of (7.5 mg of TZ + 2.00 g of Nano‐CUR/kg B.W.) which revealed mild tubular degeneration and dilatation of the glomerular capillaries. These results support the protective and therapeutic effects of Nano‐CUR on the histology of liver and kidneys and their related function biomarkers. Also, Nano‐CUR corrects the imbalance in serum glucose (sGlu), AFP, PKC, and lipid profiles in TZ‐ingested rats compared to control.