Liver Toxicity In Rats Research Articles

Hepatoprotective Effect of Quinic Acid Against Ethanol-Induced Liver Toxicity in Rats: Biochemical, Physiological, and Histological Insights

Alcohol consumption is associated with several health issues, including Alcoholic Liver Disease (ALD). Quinic acid, a cyclic polyol compound, is known for its antioxidant, anticancer, anti-inflammatory, and hepatoprotective properties. This study aims to elucidate the protective mechanisms of quinic acid against ethanol-induced liver toxicity in rats. Male rats (n=32) were divided into four groups (n=8 per group) and treated over 60 days. Group 1 received a standard diet with isocaloric glucose; Group 2 was treated with 30% ethanol daily; Group 3 received 30% ethanol and quinic acid (50 mg/kg) from day 31; Group 4 was given glucose and quinic acid from day 31. Biochemical, physiological, and histological evaluations were performed post-treatment. Ethanol-treated rats exhibited significant decreases in body weight, abnormal liver morphology, increased liver enzyme levels (AST, ALT, ALP, and GGT), disrupted lipid and renal profiles, and altered phase I and II enzyme activities. Quinic acid supplementation in ethanol-treated rats significantly reversed these changes by improving body weight, restoring liver morphology, normalizing liver enzyme activities, and maintaining lipid-lipoprotein balance and enzyme levels. Histopathological analysis demonstrated reduced liver damage in quinic acid-treated groups. Quinic acid exhibits hepatoprotective effects against ethanol-induced toxicity by reducing oxidative stress, normalizing liver functions, and preserving liver structure. These findings highlight its potential as a therapeutic agent for managing ALD.

Docetaxel-induced liver and kidney toxicity in rats can be alleviated by suppressing oxidative stress, endoplasmic reticulum stress, inflammation, apoptosis and autophagy signaling pathways after Silymarin treatment.

Approximately 20 million new cancer cases have occurred worldwide, and dose limitation occurs because of the liver and kidney toxicity of chemotherapeutic agents. Inflammation/apoptosis/ROS pathways appear to be activated in the liver and kidney toxicity of chemotherapeutic agents. This study was conducted to investigate the potential effects of silymarin (SLY) use against docetaxel (DTX)-induced liver and kidney damage in rats. For this purpose, 30mg/kg DTX was administered intraperitoneally to Sprague Dawley rats on the first day of the study, followed by SLY (25 or 50mg/kg/day) orally for 7 days. Then, various analyses were performed on liver and kidney tissues using biochemical, molecular and histological methods. The data obtained showed that DTX administration suppressed antioxidant markers and increased lipid peroxidation in liver and kidney tissues. It was also determined that DTX administration triggered markers of endoplasmic reticulum stress, inflammation, apoptosis and autophagy. On the other hand, SLY treatment increased enzymatic and non-enzymatic antioxidant levels and decreased malondialdehyde levels. Additionally, SLY alleviated DTX-induced endoplasmic reticulum stress, inflammation, apoptosis and autophagy in liver and kidney tissues. Immunohistochemical analyses showed that DTX increased the density of 8-OHdG positive cells in liver and kidney tissues, while oxidative DNA damage decreased after SLY administration. ALT, AST, ALP, Urea and Creatinine levels increased in the DTX group and decreased in the SLY treatment groups. In conclusion, DTX administration caused toxicity in liver and kidney tissues and damaged tissue integrity, while SLY treatment alleviated DTX-induced toxicity.

Regulation of TGF-β1, PI3K/PIP3/Akt, Nrf-2/Keap-1 and NF-κB signaling pathways to avert bifenthrin induced hepatic injury: A palliative role of daidzein.

Bifenthrin (BFN) is a noxious insecticide which is reported to damage various body organs. Daidzein (DZN) is a natural flavone with excellent pharmacological properties. This research was conducted to evaluate the alleviative strength of DZN to counteract BFN prompted liver toxicity in male albino rats. Thirty-two rats were divided into 4 groups i.e., the control, BFN (7 mg /kg), BFN (7 mg/kg) + DZN (20 mg/kg) and DZN (20 mg/kg) alone group. The biochemical assessment was performed by using qRT PCR as well as standard ELISA protocols. The findings are validated by applying pharmacodynamic techniques including molecular simulation. It was observed that BFN reduced the gene expressions of phosphoinositide 3-kinase (PI3K), phosphatidylinositol-3, 4, 5-triphosphate (PIP3), Protein kinase B (Akt), nuclear factor erythroid 2-related factor 2 (Nrf-2) while promoting the gene expressions of Kelch-like ECH-associated protein 1 (Keap-1). Moreover, BFN notably reduced the activities of glutathione reductase (GSR), heme-oxygenase-1 (HO-1), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) while elevating the levels of reactive oxygen species (ROS) and malondialdehyde (MDA). BFN promoted the levels of matrix metallopeptidase 2 (MMP-2), Procollagen III N-terminal Pro-peptide (PIIINP), alkaline phosphatase (ALP), transforming growth factor-beta-1 (TGF-β1), aspartate aminotransferase (AST), tissue inhibitor of matrix metalloproteinases 1 (TIMP1), and alanine aminotransferase (ALT). The levels of nuclear factor- kappa B (NF-κB), interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and cyclooxygenase-2 (COX-2) were increased following the BFN intoxication. BFN enhanced the expressions of cysteine-aspartic acid protease-3 (Caspase-3) and Bcl-2-associated X protein (Bax) while suppressing the gene expression of B-cell lymphoma-2 (Bcl-2). Moreover, BFN disrupted the normal histology of liver tissues. Nonetheless, DZN treatment remarkably alleviated hepatic damages owing to its antioxidative, anti-apoptotic as well as anti-inflammatory abilities. However, DZN supplementation remarkably safeguarded which is further confirmed by in-silico assessment.

Evaluation of L-carnitine's protective properties against AlCl3-induced brain, liver, and renal toxicity in rats.

A common heavy metal in many facets of daily life is aluminum (AlCl3), which can be found in food, toothpaste, cosmetics, food additives, and numerous pharmaceutical items. The hippocampus, liver, and kidneys have the highest concentrations of this powerful neurotoxin, which also accumulates over time and contributes to the development of a number of cognitive disorders. Long-term overconsumption of AlCl3 results in hepatic and renal toxicity as well as neuronal inflammation. The purpose of the research is to assess the potential protective effects of various L-carnitine dosages as an antioxidant against hebato, renal, and neuronal toxicity in rats caused by aluminum chloride (AlCl3) (20 mg/kg, 1/20 LD 50). Six groups (n = 6), consisting of 36 adult albino rats, were randomly assigned. Saline was administered to the control group (GI) by injection. (GII) had given an injection of L-carnitine at a low-dose of 75 mg/kg body weight. An injections of L-carnitine at a high-dose (150 mg/kg) were given to (GIII), and AlCl3 (20 mg/kg) was given to (GIV). (GV) administered with L-carnitine (75 mg/kg) and AlCl3 (20 mg/kg) by injection. For 60 days, AlCl3 (20 mg/kg) and L-carnitine (150 mg/kg) were administered to GVI by injection. Furthermore, the histological structure of the cortex, hippocampus, and hepatic renal tissues appeared to change in response to AlCl3. L-carnitine therapy lessened the negative effects of AlCl3. The observable improvement in the tissues of the brain, liver, and kidneys further supported this histopathologically. It is possible to draw the conclusion that L-carnitine holds promise as a corrective measure for AlCl3, which causes renal toxicity and neural hepatotoxicity in rats. When it comes to adult albino rats, L-carnitine has a negative impact and exhibits ameliorative effects against aluminum chloride.

Investigating the effects of equeous fruit extract of <i>Tamarindus indica</i> on mercuric chloride-induced liver toxicity in adult Wistar rats

Investigating the effects of equeous fruit extract of <i>Tamarindus indica</i> on mercuric chloride-induced liver toxicity in adult Wistar rats

Pharmacotherapeutic potential of pratensein to avert metribuzin instigated hepatotoxicity via regulating TGF-β1, PI3K/Akt, Nrf-2/Keap-1 and NF-κB pathway

Metribuzin (MBN) is a selective herbicide that adversely damages the vital organs of the body including the liver. Pratensein (PTN) is a novel flavonoid that exhibits marvelous medicinal properties. This experimental trial commenced to elucidate the pharmacotherapeutic strength of PTN to counteract MBN provoked liver toxicity in rats. Thirty-six male albino rats (Rattus norvegicus) were categorized into four groups i.e., the control, MBN (133.33 mg/kg), MBN (133.33 mg/kg) + PTN (20 mg/kg) and PTN (20 mg/kg) alone treated group. Our findings revealed that MBN exposure promoted the expressions of Keap-1 as well as concentrations of ROS and MDA while reducing the gene expressions of Nrf-2 as well as activities of catalase (CAT), glutathione Peroxidase (GPx), glutathione reductase (GSR), heme oxygenase-1 (HO-1), superoxide dismutase (SOD) and glutathione (GSH) contents. The levels of albumin and total proteins were reduced whereas the levels of alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were enhanced following the MBN administration. Moreover, the gene expression of transforming growth Factor–β1 (TGF-β1), matrix metallopeptidase-2 (MMP-2), matrix metallopeptidase-9 (MMP-9), collagen, type I, alpha 1 and type-3 alpha were escalated in response to MBN intoxication. Furthermore, MBN administration cause a sudden upregulation in the levels of NF-κB, IL-1β, TNF-α, IL-6 & COX-2. Besides, MBN exposure enhanced the gene expression of Bax and Caspase-3 while reducing the gene expression of PI3K, Akt and Bcl-2. Additionally, MBN exposure dysregulated the normal histology of liver. However, PTN treatment notably protected the hepatic tissues via regulating abovementioned dysregulations due to its marvelous ROS scavenging potential.

Effects of Remdesivir on Liver Enzymes, Oxidative Stress and Liver Histopathology in Rats

<i>Background & Aims:</i> Remdesivir (REM) has been widely used to treat subjects affected by COVID-19 due to its broad-spectrum activity. The aim was to assess the REM effect on liver histopathology, enzymes, and alterations in oxidative stress markers. <i>Methods:</i> Forty-eight Wistar rats were separated into eight groups as follows: Group A (Control) received normal saline intraperitoneally (IP) for 10 days; Group B (Low-dose REM) received REM (2.8 mg/kg for the first day and 1.4 mg/kg for days 2 to 10, IP); Group C (High-dose REM) received REM (8.5 mg/kg IP for the first 17 days and days 2 to 10); Group D (High-dose REM+DEX (Dexamethasone)+ HEP (Heparin) received DEX (7 mg/kg intramuscularly for 10 days) and HEP (333 IU/kg subcutaneously on the first day and 250 IU/kg subcutaneously every 12 hours from day 2 to day 10); Group E (High-dose REM+ DEX); Group F (High-dose REM+ HEP); Group G (DEX); Group H (HEP). For statistical analysis, non-parametric tests (Kruskal-Wallis H and Mann-Whitney U) were used for pathological lesions (semi-quantitative data) between the different groups, and a p < 0.05 was considered significant. <i>Results:</i> There were mild to severe pathological changes in the treated groups, including cell swelling, vascular congestion. Also, the D and G groups showed similar pathological lesions, which were more severe than in other treated groups with a significant difference (p < 0.05). Conclusions: This study identified Remdesivir-induced liver toxicity and oxidative stress alterations in rats, underscoring the need for careful liver function monitoring, especially in patients with hepatic dysfunction. The findings recommend caution in using Remdesivir as a first-line treatment in such cases, and further studies are required to validate these effects and explore broader clinical implications.

Inhibitory activity of nanoencapsulated quercetin against sodium arsenite-induced sub-acute liver toxicity in rats

Arsenic, a metalloid toxicant, is associated with a major global health problem as oxidative stress, a prime cause of tissue toxicity. The subject of our investigation was to assess the therapeutic efficiency of nanoencapsulated quercetin (QC) in combating sodium arsenite (NaAsO2)-inducted sub-acute hepatocellular toxicity in rat model. The rats of the hepatic damage group were injected subcutaneously (s.c.) four dosages of NaAsO2 (92.36 µM/kg b.wt.) twice a week. The rats of the polylactide nanoencapsulated QC group were injected intravenously (i.v.) four doses of nanoencapsulated QC (8.97 µmol/kg b.wt.) twice a week 2 h after the treatment (s.c.) with 92.36 µM /kg b. wt. NaAsO2 twice a week for four doses. The rats of the empty nanocasule or free QC treated group were injected i.v. four doses empty nanocapsule or free QC twice a week 2 h after the treatment (s.c.) with same doses of NaAsO2 twice a week for four doses. Arsenic deposition (580±20 µg/g protein) observed in liver tissue of rats treated with arsenite (92.36 µM/kg b.wt.), was found to reduce (120±9 µg/g protein) by the treatment of nanoencapsulated QC in rats significantly (p<0.001). The levels of antioxidant enzymes and GSSG/GSH ratio enhanced (p<0.001/0.1/0.01) by the treatment of NaAsO2 were reduced by the post treatment of nanoencapsulated QC significantly (p<0.001/0.01). The levels of ROS, lipohydroperoxide or membrane microviscosity increased or decreased (p<0.001) by the treatment of NaAsO2 were monitored to reduce or enhance significantly (p<0.001) by the treatment of nanoencapsulated QC in rat liver respectively. The blood serum biochemical levels enhanced (p<0.001) by the treatment of NaAsO2 were found to reduce significantly (p<0.001) by the treatment of nanoencapsulated QC in rats. The TGFβ1 and MMP-13 in the rat plasma augmented (p<0.001) by the treatment of NaAsO2-exposure were found to decline (p<0.001) significantly by the treatment of nanoencapsulated QC in rats. The rats in the other groups such as empty nanocapsule or free QC treated showed no or less inhibitory efficiency against NaAsO2-treatment compared to nanoencapsulated QC treated group. Application of nanoencapsulated QC may be a potent formulation to get higher inhibitory therapeutic efficiency against NaAsO2-induced sub-acute hepatocellular toxicity.

Sophoricoside reduces inflammation in type II collagen-induced arthritis by downregulating NLRP3 signaling

Immune responses, especially NLRP3 signaling in macrophages, play critical roles in rheumatoid arthritis (RA), an autoimmune and inflammatory disease. In this study, we aimed to identify novel therapies for RA. We focused on sophoricoside (SOP), an isoflavone glycoside isolated from Sophora japonica. We predicted the targets of SOP and performed a Gene Ontology analysis to assess its effects. The results suggested that SOP is related to inflammation regulation. We verified these findings by performing in vitro experiments with M1 macrophages differentiated from human peripheral blood monocytes (THP-1 cells). Sophoricoside administration reduced inflammatory activity and NLRP3, Caspase-1, and IL-1β protein levels in macrophages. In addition, SOP and triptolide (TP) was administered intragastrically to male SD rats (n = 40) in a collagen-induced arthritis model. We observed that SOP and TP reduced the inflammatory responses and symptoms of RA. Moreover, unlike TP, SOP showed no liver or kidney toxicity in rats. In conclusion, SOP reduces inflammation in type II collagen-induced arthritis by downregulating NLRP3 signaling and has potential for future clinical applications as an ideal therapy for RA.

Assessment of sweet whey fortified with Bifidobacteria and selenium on reduction of pesticide liver toxicity in albino rats

Deltamethrin (DLM) represents one of the most commonly used pesticides. It passes through milk, vegetables, and fruits to humans or through animals (veterinary drugs and feeding on contaminated forage) to milk; it can escape from skin to blood and be secreted in breast milk in lactating women. It is believed to have neurotoxic, nephrotoxic, and hepatotoxic properties. To investigate deltamethrin-induced hepatotoxicity, 64 rats were divided into eight groups. The control group did not receive any treatment. The groups were as follows: D 30 mg DLM/kg body weight (BW) dissolved in corn oil; B 1 mL whey (1010 cfu/mL of Bifidobacterium longum ATCC 15707); S 1 mL whey (0.5 ppm selenium); BS 1 mL whey (1010 cfu/mL of B. longum ATCC 15707 + 0.5 ppm selenium); BD 1 mL whey (1010 cfu/mL of B. longum ATCC 15707 + DLM); SD 1 mL whey (0.5 ppm selenium) + DLM; and BSD 1 mL whey (1010 cfu/mL of B. longum ATCC 15707) + 0.5 ppm selenium + DLM. Results revealed that the manipulation of Bifidobacteria with selenium triggered a significant improvement in AST (U/mL), ALT (U/mL), GSH (mg/g), TNF-α (pg/mL), NF-κB (ng/mL), and BCL2 (ng/mL) from 166.7 ± 6.42, 30.67 ± 0.55, 0.252 ± 0.005, 17.18 ± 0.42, 1.14 ± 0.10, and 1.77 ± 0.06 versus 334.9 ± 4.7, 72.83 ± 2.49, 0.108 ± 0.005, 33.57 ± 0.59, 2.58 ± 0.05, and 1.04 ± 0.04, respectively, compared to DLM group. As well as reduction in histopathological necrosis, congestion, and degradation. Whey beverages fortified with B. longum and selenium implicated a reduction in oxidative stress and histopathological degradation that accomplished DLM toxicity. The utilization of whey (a byproduct of cheese making) is considered a recycling process that supports eco-friendly practices and sustainability, thus encouraging its use as a protective tool in animal feed or manipulation by humans, especially workers in pesticide plants.

Hepatoprotective activity of aqueous <i>Curcuma longa</i> rhizome extract against carbon tetrachloride-induced liver toxicity in adult Wistar rats

Hepatoprotective activity of aqueous <i>Curcuma longa</i> rhizome extract against carbon tetrachloride-induced liver toxicity in adult Wistar rats

Hepatoprotective effects of resveratrol on α-amanitin-induced liver toxicity in rats

ObjectiveThe hepatoprotective effects of resveratrol against α-Amanitin (α-AMA)-induced liver toxicity were investigated in an experimental rat model, focusing on oxidative stress, inflammation, apoptosis, and liver function. MethodsThirty-two male Sprague-Dawley rats were divided into four groups (n = 8 per group): Control, resveratrol, α-AMA, and resveratrol+α-AMA. The resveratrol group received 20 mg/kg resveratrol orally for 7 days. The α-AMA group received 3 mg/kg α-AMA intraperitoneally on the 8th day. The resveratrol+α-AMA group received 20 mg/kg resveratrol orally (7 days) followed by 3 mg/kg α-AMA intraperitoneally on the 8th day. Liver tissues and blood samples were collected 48 h after α-amanitin administration for histopathological, immunohistochemical (NFkB, LC3B), and biochemical analyses (GSH, MDA, CAT, GPx, MPO, NOS, AST, ALT). Resultsα-AMA significantly increased AST and ALT levels, oxidative stress marker (MDA), and inflammatory marker (MPO), while reducing antioxidant levels (GSH, CAT, GPx) and NOS concentration (P < 0.001 for all parameters). Histopathological analysis showed severe liver damage with increased NFkB and LC3B expression. resveratrol treatment significantly reduced AST and ALT levels (P < 0.01 for both parameters), decreased MDA and MPO levels, and increased NOS concentration, GSH, CAT, and GPx levels (P < 0.05 for all parameters). Reduced NFkB and LC3B expression in the resveratrol+α-AMA group and showed histopathological improvements. ConclusionResveratrol demonstrated substantial hepatoprotective effects against α-AMA induced liver toxicity by reducing oxidative stress, inflammation, and apoptosis, and improving liver function. These findings suggest that resveratrol could be a potential therapeutic agent for treating liver damage caused by potent hepatotoxins like α-AMA.

Pharmacotherapeutic potential of malvidin to cure imidacloprid induced hepatotoxicity via regulating PI3K/AKT, Nrf-2/Keap-1 and NF-κB pathway

Imidacloprid (IMI) is one of the top-notch insecticides that adversely affects the body organs including the liver. Malvidin (MAL) is a natural flavonoid which exhibits a wide range of pharmacological properties. This research was designed to evaluate the protective ability of MAL to counteract IMI instigated liver toxicity in rats. Thirty-two rats were divided into four groups including control, IMI (5mg/kg), IMI (5mg/kg) + MAL (10mg/kg) and MAL (10mg/kg) alone treated group. The recommended dosages were administrated through oral gavage for 4 weeks. It was revealed that IMI intoxication disrupted the PI3K/AKT and Nrf-2/Keap-1 pathway. Furthermore, the activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), heme-oxygenase-1 (OH-1) and glutathione reductase (GSR) were reduced while upregulating reactive oxygen species (ROS) and malondialdehyde (MDA) levels after IMI treatment. Moreover, IMI poisoning increased the levels of ALT (Alanine aminotransferase), AST (Aspartate transaminase), and ALP (Alkaline phosphatase) while reducing the levels of total proteins and albumin in hepatic tissues of rats. Besides, IMI administration escalated the expressions of Bcl-2-associated protein x (Bax) and cysteine–aspartic acid protease-3 (Caspase-3) while downregulating the expressions of B-cell lymphoma 2 (Bcl-2). Similarly, IMI intoxication, increased the levels of Interleukin-6 (IL-6), Nuclear factor kappa-B (NF-κB), Interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and the activity of cyclooxygenase-2 (COX-2). Furthermore, IMI disrupted the normal architecture of hepatic tissues. However, MAL treatment remarkably protected the liver tissues via regulating abovementioned disruptions.

DETERMINATION OF ANTIOXIDANT ACTIVITY OF HIPPOPHAE RHAMNOIDES L. GROWING IN TURKEY AND INVESTIGATION OF ITS EFFECTS ON THE LIVER TOXICITY IN RATS

Objective: The goal of the present work was to investigate the antioxidant properties of the extracts of Hippophae rhamnoides L. and to determine their effects on liver toxicity in rats. Material and Method: Metal chelation, reducing power and DPPH radical scavenging methods were used in the antioxidant activity analysis of extracts. The total phenolic content was determined using the folin-ciocalteu reagent. Plant extracts were administered orally to the rats at doses of 500 µg/kg for 2 days. Each animal group was composed of six female Albino Wistar rats with an average weight of 250 g. Microscopic examination was carried out to observe any pathological changes in the rat livers. Result and Discussion: Water extract showed the highest radical scavenging activity (48.65%), reducing power (0.291 absorbance at 700 nm) and metal chelating (35.40%) at 1 mg/ml concentration. Histopathological studies showed that especially water extract reduced the severity of CCl4-induced intoxication. Hippophae rhamnoides L. extracts were found to have antioxidant activity, and also Hippophae rhamnoides L. water extract was shown to be particularly effective in preventing liver damage.

The Potential Effects of Cake Fortified with Date Seeds against Aflatoxin B1-Induced Liver Toxicity in Rats

The Potential Effects of Cake Fortified with Date Seeds against Aflatoxin B1-Induced Liver Toxicity in Rats

Therapeutic potential of salvigenin to combat atrazine induced liver toxicity in rats via regulating Nrf-2/Keap-1 and NF-κB pathway

Atrazine (ATR) is the second most extensively used herbicide which adversely affects the body organs including liver. Salvigenin (SGN) is a flavonoid which demonstrates a wide range of biological and pharmacological abilities. This study was planned to assess the protective ability of SGN to avert ATR induced liver damage in rats. Thirty-two rats (Rattus norvegicus) were divided into four groups including control, ATR (5 mg/kg), ATR (5 mg/kg) + SGN (10 mg/kg) and SGN (10 mg/kg) alone supplemented group. ATR exposure reduced the expression of Nrf-2 while instigating an upregulation in Keap-1 expression. Furthermore, the activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), heme‑oxygenase-1 (HO-1) and glutathione reductase (GSR) contents were decreased while increasing reactive oxygen species (ROS) and malondialdehyde (MDA) levels after ATR treatment. Moreover, ATR poisoning increased the levels of ALT, AST, and ALP while reducing the levels of total proteins, and albumin in hepatic tissues of rats. Besides, ATR administration escalated the expressions of Bax and Caspase-3 while inducing a downregulation in the expressions of Bcl-2. Similarly, ATR intoxication increased the levels of Interleukin-6 (IL-6), Nuclear factor kappa-B (NF-κB), Interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and the activity of cyclooxygenase-2 (COX-2). Furthermore, ATR disrupted the normal histology of hepatic tissues. However, SGN treatment remarkably protected the liver tissues via regulating antioxidant, anti, inflammatory, anti-apoptotic as well as histology parameters. Therefore, it is concluded that SGN can be used as therapeutic agent to combat ATR-induced hepatotoxicity.

Protective effects of cupressuflavone against doxorubicin-induced hepatic damage in rats

Doxorubicin (DOX) is a potent chemotherapeutic agent that is used in various sorts of malignancies. However, its uses are restricted owing to its deleterious effects on different organs including the liver. Cupressuflavone (CUP) is a plant-based flavonoid which is well known for its biological as well pharmacological potential. Our investigation aimed to evaluate the ameliorative potential of CUP against DOX provoked liver toxicity in rats. Twenty-four albino rats (Rattus norvegicus) were distributed into four distinct groups such as control, DOX (3 mg/kg), co- administrated DOX (3 mg/kg) + CUP (40 mg/kg) and CUP (40 mg/kg) only. DOX exposure reduced catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), Glutathione reductase (GSR), glutathione-S-transferase (GST) activities and glutathione (GSH) content while escalating the levels of reactive oxygen species (ROS) and malondialdehyde (MDA). Besides, the levels of ALT, AST and ALP were increased in response to DOX exposure. Furthermore, administration of DOX upregulated the levels of Interleukin-6 (IL-6), Nuclear factor kappa-B (NF-κB), Interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and the activity of cyclooxygenase-2 (COX-2). The treatment of DOX reduced the levels of Bcl-2 while escalating the levels of Caspase-3, Caspase-9 and Bax. Similarly, DOX intoxication instigated various histopathological disruptions in hepatic tissues of rats. However, supplementation of CUP notably (p < 0.05) restored abovementioned hepatic dysregulations owing to its anti-oxidative, anti-inflammatory as well as anti-apoptotic potential. Our results manifested that CUP could be used as hepatoprotective agent againt DOX induced liver damage in rats.

Biochemical, morphological and molecular assessments of n butanol fraction of Phoenix dactylifera L. following exposure to inorganic mercury on the liver of Wistar rats

BackgroundMercury chloride (HgCl2) damages tissues it comes in contact with in sufficient concentration. This study evaluated the protective effects of n-butanol fraction of Phoenix dactylifera (BFPD) on mercury-triggered liver toxicity in Wistar rats. 25 male rats were divided into 5 groups of 5 rats each. Group I was administered 2 ml/kg of distilled water; group II was administered 5 mg/kg of HgCl2; group III was administered 500 mg/kg of BFPD + 5 mg/kg of HgCl2; group IV was administered 1000 mg/kg of BFPD + 5 mg/kg of HgCl2, while group V was administered 100 mg/kg of silymarin + 5 mg/kg of HgCl2. orally for 2 weeks. The rats were euthanized and liver tissue blood samples were collected for histological, histochemical, stereological, immunohistochemical, molecular, and biochemical studies.ResultsThe results revealed that HgCl2 induced oxidative stress in the rats evident by histoarchitectural distortions and altered levels of liver enzymes, proteins, and oxidative stress biomarkers when compared to the control. However, BFPD treatment restored these changes. Glutathione peroxidase levels decreased (p < 0.05) in the HgCl2−treated group when compared to the control and BFPD-treated groups. HgCl2 group revealed reduced reactivity with histochemical and immunohistochemical stains (Masson’s Trichrome and B cell Lymphoma 2) when compared to the control, with a significant decrease in quantified liver Bcl-2 stain intensity when compared to the silymarin-treated group. BFPD administration revealed normal staining intensity comparable to the control. HgCl2 administration revealed a remarked decrease in the number of hepatocytes when compared to the control, BFPD, and silymarin groups. BFPD preserved (p < 0.05) the stereological features when compared to the HgCl2-treated group. GPx activity in the liver decreased (p < 0.05) with HgCl2 administration when compared to the control and silymarin-treated groups. BFPD attenuated GPx gene activity to levels similar to the control indicating some level of amelioration against HgCl2-induced toxicity.ConclusionsThe ability of BFPD to mitigate HgCl2 triggered liver alterations could be attributed to the antioxidant property of its flavonoid content. Therefore, BFPD may be a potential candidate for treating and managing liver-induced mercury intoxication.

Hepato-protective Effect of Costus afer (Okpete) Juice Extract on Alcohol-induced Liver Toxicity in Adult Female Wistar Rats

Background: The oral intake of alcohol has become a widespread concern due to its high risk to body health. Therefore, our purpose in this study was to reveal the antioxidant efficacies of natural Costus's afer stem juice extract on hepatotoxicity induced by ethanol in adult female wistar rats. Methods: We examined the impacts of liver toxicity, were the experimental animals were given 1ml of 10% ethanol daily for 21 days, thereafter, C. afer was administered to evaluate its ameliorative effect in the female albino wistar rats orally treated with C. afer juice extract (200 and 400 mg/kg) for 7days. The rats were divided into four (4) groups; Group A served as the control group, which was given rat chow and water only. Groups B, C and D were given 1ml of 10% ethanol. Afterwards, groups C and D were treated with 200 and 400 mg/kg using 1ml and 2ml of the juice extract of C. afer, respectively. A liver function test and histological analysis were carried out. Results: The results showed that treatment with C. afer after the oral consumption of ethanol caused elevation in serum liver function parameters (alanine transferases, aspartate transaminase, and alkaline phosphate), which is significant compared to the control group. There was also a slight restoration in histopathological changes in the liver, as revealed by decreased areas of inflammation. Conclusion: The therapeutic efficiency of C. afer juice extract could be due to traces of anti-inflammatory properties and the ROS-scavenging agent. Our findings prove that the elevation of liver function markers by C. afer enables hepatic tissue to suppress inflammatory and oxidative mechanisms, resulting in enhanced liver structure and function. Therefore, C. afer extract is a protective and therapeutic supplement against toxic agents.

Metabolic profiling of Verbena bonariensis L. extract by LC/MS and evaluation of the hepatoprotective potential with isoniazid- and rifampicin-induced hepatotoxicity in rats.

The study explored the hepatoprotective activity and metabolic profile of Verbena bonariensis L. methanol extract (VBM) and fractions using isoniazid as well as rifampicin-triggered liver toxicity in Wistar albino rats. Metabolite profiling of VBM using HPLC-PDA-ESI-MS identified 12 compounds, mainly iridoids, phenylpropanoids, and flavonoids, where verbascoside represents the major compound. Different biochemical parameters such as aspartate transaminase (AST), alanine transaminase (ALT), and alkaline phosphatase (ALP), bilirubin, and total protein levels were used to assess liver functions. All the evaluated samples exhibited hepatoprotective potential, but VBM exhibited maximum activity and a notable decline in ALP (p < 0.05, significant), even better than the standard drug (silymarin). VBM significantly reduced the elevated ALT, AST, ALP, and total bilirubin. It also triggered a significant elevation in total proteins compared with diseased animals. This was further consolidated by histopathological studies. Verbena bonariensis L. could serve as a potent hepatoprotective agent and may alleviate liver ailments.