Levels Of Serum Marker Enzymes Research Articles

ASERUM BIOCHEMICAL PROFILES AND IMMUNO-STIMULATORY POTENTIALS OF Clarias gariepinus JUVENILES FED FISH MEAL CONTAINING DIFFERENT INCLUSION LEVELS OF Sesame indicum SEED MEAL

Sesame indicum L. is a class of the Pedaliaceae family of plants that contains good eatable oil, protein, mineral (calcium), and antioxidants and has been recommended as good food for ages. Beni seeds possess a nutritional content that is favour of digestibility, growth, and feed utilization among domesticated animals. The serum biochemical profiles and immunostimulatorypotentials of Clarias gariepinus juveniles fed Sesame indicum seed meal-based diets were carried out. Serum marker enzymes (ALT, AST, ALT, GGT, and LDH), serum chemistry; {glucose (GLU), total protein (TPN), bilirubin (BIL), cholesterol (CHL), albumin (ALB), creatinine (CTN), and immuno-stimulatory potentials; haemoglobin (Hb), packed cell volume (PCV), white blood cells (WBC), lymphocytes (LYM), neutrophils (NEU), monocytes (MON), eosinophil (EOS), and basophils (BAS) in C. gariepinus fed Sesame indicum seed meal-based diets were serum biochemical indices analyzed. High levels of serum marker enzymes {ALT (18.12-22.43U/L), AST (20.13-20.57U/L), ALT (18.62-22.65U/L), GGT (1.72-2.40U/L), LDH (104.35-110.01U/L)}, serum chemistry {Glucose (72.42- 75.34mg/dL), protein (7.01-7.04g/dL), bilirubin (0.44-1.52mg/dL), cholesterol (77.22-82.02mg/dL), albumin (2.46-3.65g/dL),creatinine (0.16-0.23mg/dL), and immuno-stimulatory potential (not greater than the permissible level) were observed in C. gariepinus fed S. indicum seed meal-based diets compared to those fed the control diet (DT1) only. Based on these results, the inclusion of S. indicum in the diets of C. gariepinus could therefore be saved and look promising in terms of health benefits.

Investigation on Potential Efficacy of Methanol Extract of Lawsonia inermis L. against Carbon Tetrachloride Induced Hepatotoxicity in Wistar Albino Rats

Carbon tetrachloride (CCl4) a pharmacological tool was used to induce liver damage in Wistar albino rats. Silymarin (100 mg/kg) and methanol extract of Lawsonia inermis Linn. family Lythraceae (known to possess hepatoprotective compounds) was used to reverse the liver damage caused due to CCl4 (induced toxicity). Hydroalcholic extract of stem bark and leaf of Lawsonia inermis Linn. was evaluated, for its restorative efficacy against CCl4 induced hepatotoxicity which was assessed in terms of biochemical and histopathological parameters. CCl4 produce the altitude levels of serum marker enzymes of alanine aminotransferase (ALT), asparate aminotransferase (AST), alanine phosphatase (ALP) and bilirubin in blood serum. Due to the toxicity of CCl4 cause turbine hepatic cell architecture, necrosis, inflammatory cell infiltration, congestion, and sinusoidal dilatation along with reduction of superoxide dismutase (SOD), catalase, Glutathione-S-transferase (GST) and glutathione peroxidase (GPx) appeared in liver tissue. SOD is the primary step in the defense mechanism involved in the antioxidant system against the oxidative stress. It diminishes by converting the superoxide radical in to peroxide and molecular oxygen. CAT or GPx reactions, also exert a similar effect thereby reducing the level of cellular damage. By oral administration of methanol extract of Lawsonia inermis Linn. plant extracts, i.e., stem bark extract (250 mg/kg b.wt.) and leaf extract (250 mg/kg b. wt.) the levels of these parameters was restored to near controlled (untreated) levels. Thus, the present study revealed that the extracts of stem bark and leaf of Lawsonia inermis Linn. offered protection against hepatotoxicity induced by CCl4.

Hepatoprotective Potential of Tecomella undulata Bark on Paracetamol and CCL4 Induced Hepatotoxicity in Rats: Invitro Analysis

In this study the T. undulata bark was tested for its hepatoprotection against paracetamol (PCM) induced hepatic damage and Carbon tetra chloride (CCl4) induced hepatotoxicity. The Invitro study was performed on HepG2 cell line .The Levels of serum marker enzymes i.e. AST, ALT (aminotransferases), ALP (alkaline phosphatase), GSH (reduced glutathione) and MDA (Malondialdehyde) in 70% Ethanol treated rats were monitored, respectively. The 70% Ethanol extract gave promising results as studied in detail. The Present study showed that the 70 % ethanolic extract of bark of T.undulata apparently revive the physiological integrity of hepatocytes. Thus the present study demonstrated the Hepatoprotective property of Tecomella undulate Bark.

Curative Effects of Aqueous and Ethanol Stem Bark Extracts of Vitex doniana on Doxorubicin-Induced Cardiotoxicity in Rats

Background: Cardiovascular diseases (CVDs) constitute the number one cause of mortality at the global level, representing 30% of all global deaths. Therefore, finding ways to reduce deaths due to CVDs remain an important public health goal. Traditional healers in northern Nigeria use the stem bark of Vitex doniana to treat hypertensive patients. This study was aimed to investigate the cardiocurative potential of Vitex doniana on doxorubicin-induced Cardiotoxicity in rats.
 Methods: Thirty five (35) adult Albino rats weighing 175 ± 25 g were used, of which 30 were induced with cardiotoxicity by intraperitoneal injection of doxorubicin (10 mg/kg) for three consecutive days. Rats were treated by oral administration of Silymarin (100 mg/kg) and Vitex doniana aqueous or ethanol extract (100 mg/kg and 200 mg/kg) for 14 consecutive days and thereafter were sacrificed on the 15th day. Blood, plasma and serum were analyzed for lipid profile and serum markers for cardiotoxicity.
 Results: Phytochemical analysis of the extracts showed the presence of alkaloids, tannins, flavonoids, steroids, phenols, saponins, terpenoids and glycosides. Oral treatment with Vitex doniana extracts significantly (p<0.05) lowered the elevated levels of total cholesterol, triglycerides and LDL but significantly (p<0.05) increased the level of HDL (18.61 ± 0.55 mg/dl to 57.98 ± 0.78 mg/dl). The extracts also significantly (p<0.05) decreased the levels of serum marker enzymes for cardiotoxicity ALT, AST, CK – mb and LDH.
 Conclusion: The prophylactic cardiocurative use of Vitex doniana stem bark has been confirmed in this study as the extracts exhibited hypolipidemic and cardiocurative effects in dose dependent manner in doxorubicin-induced cardiotoxicity rat model.

Hepatoprotective Activity of Citrus Limetta on Wistar Albino Rats Hrishabh Jangid*, Mohammad Mukim, Rahul Ancheria, Ankit Sharma Kota College of Pharmacy, Kota, Rajasthan, India

The methanolic extract of citrus limetta (MECL) peel was screened for hepatoprotective activity in hepatotoxic wistar albino rats induced via paracetamol (PCM) and carbon tetra chloride (CCL4). Hepatoprotective activity of MECL was measured by estimating biochemical parameters such as AST (aspartate transaminase), ALT (alanine aminotransferase), SGPT (serum glutamine pyruvate transferase), SGOT (serum glutamic oxaloacetic transaminase). It was observed that administration of PCM, CCL4 decrease the level of proteins and increased the level of serum marker enzymes which is an evidence of existence of hepatotoxicity in rats. The present results provide strong evidence that MECL inhibits hepatotoxicity induced by CCL4 and PCM. The hepatoprotective action was much more significant at the dose of 2ml/kg when compared to 1mg/kg.

Quercetin with lycopene modulates enzymic antioxidant genes pathway in isoproterenol cardiotoxicity in rats

ABSTRACT Quercetin (QN) is a naturally occurring phenolic compound found largely in vegetables and fruits. Lycopene (LY) is yet another natural phytocompound, found abundantly in red-colored fruits and vegetables. Both have been reported to have beneficial activities in humans. In this study, we document in vivo experimental model for isoproterenol (ISO) cardiac injury toxicity in Sprague-Dawley (SD) rats and treatment with a combined optimized concentration of quercetin and lycopene (QL). Male SD rats of different groups were treated with QL (80 mg/kg QN and 3 mg/kg LY together p.o.) for 10 days with ISO administration (100 mg/kg i.p.) on days 7 and 8. After experimental period, CK-MB, TROP, AST, ALT, LDH, GST, GPx, CAT, SOD, Vit.E, Vit. C, GSH, GSSG and MDA were estimated. SD rats administered with ISO showed an obvious rise in the serum marker enzyme levels and tissue oxidative stress markers (MDA and GSSG). Furthermore, marked reductions in the body weight and increases enzymic and non-enzymic antioxidant levels were noticed. Histological features of the heart also indicated a disruption in the cardiac myofibrils structure of ISO-intoxicated rats. Also, quantitative PCR analysis revealed an involvement of antioxidant and related pathway genes such as Nrf2, HO-1, NQO1, GSTµ, SOD1, SOD2, CAT and BCl-2 genes. QL pretreatment prevented all these adverse effects of ISO cardiotoxicity and significantly reduced the myocardial damage. Decrease in oxidative stress was observed, possibly through alterations in the expression levels of enzymic antioxidant genes (GSTµ, SOD1, SOD2 and CAT). In general, QL exert a strong protective effect through the modulations in enzymic antioxidant activity and associated molecular pathways-regulating effect in cardiovascular disease.

Elucidation of malachite green induced behavioural, biochemical, and histo-architectural defects in Cyprinus carpio, as piscine model

Colours are an indispensable portion of human survival. Malachite green (MG) is a dye with a bright hue of green, used in textile, paint, and confectionery industry. For the present study, healthy fingerlings of Cyprinus carpio were exposed to sub-lethal concentration (0.087 ​mg/L) of malachite green for 15, 30, and 60 days. Assessment of chronic toxicity was made through varied organs (cornea, erythrocytes, and liver) and analytical methods, comprising behavioural, histopathological, ultra-structural (transmission electron microscopy), biochemical (antioxidant and marker enzymes) and bioaccumulation studies. Behavioural aspects, comprised of opercular and fin (dorsal and caudal) movements, presented an inverse relation with MG treatment, and displayed escaping behaviour from the experimental tank. Scanning electron microscopy (SEM) of MG exposed fish peripheral erythrocytes demonstrated morphological anomalies in form of clubbing, budding, and appearance of the varied shaped cells as stomatocytes, acanthocytes, dacrocytes and fusiform cells in the exposure dependent manner, instead of regular elliptical erythrocytes in control. Corneal epithelium study conducted through SEM in MG treated fish reported damaged pavements cells, microridges, and microplicae, and increased intra-microplicae distance compared to control fish. Elevated levels of serum marker enzymes and disturbed levels of antioxidant enzymes were also evident; accompanied by abundance of MDA-TBARs level suggestive of oxidative stress in MG treated fish. Bioaccumulation studies conducted revealed up to 3.06 fold dye deposition, conferring the enhanced and prolonged toxicity of the dye in the fish. Consequently, MG can be inferred as a strong cellular toxicant even at sub-lethal concentration.

Pomegranate Juice Diminishes The Mitochondria-Dependent Cell Death And NF-kB Signaling Pathway Induced By Copper Oxide Nanoparticles On Liver And Kidneys Of Rats.

BackgroundPomegranate (Punica granatum L) has been used since ancient times in the traditional medicine of several cultures, particularly in the Middle East. It is an essential commercial crop full of bioactive compounds with several medical applications. Pomegranate is very popular for its biological effects exerted by phenolic compounds via free radical scavenging abilities. It has revealed high antioxidant and anti-inflammatory activities and is beneficial for the amelioration of liver and kidney diseases.PurposeTo elucidate the potential efficacy of pomegranate juice (PJ) against copper oxide nanoparticles (CuO-NPs)-induced apoptosis, inflammation, and oxidative stress damage.Study design37 nm sized CuO-NPs were prepared by precipitation method and characterized by using X-ray diffractometer (XRD), Zetasizer nano-and high-resolution transmission electron microscope (HR-TEM). 30 Wistar rats were partitioned into 6 equal groups as follows: Group 1 (negative control), groups 2 & 3 (PJ control groups), group 4 (CuO-NPs group), groups 5 & 6 (CuO-NPs + PJ groups). Methods: Hepato-renal protective effect of PJ was evaluated by measuring levels of serum marker enzymes (ALT, AST,blood urea nitrogen and creatinine). Cu NPs bioaccumulation in liver and kidneys was determined by using atomic absorption spectrophotometer. The oxidative stress markers, Rt-PCR analysis, histopathological and immunohistochemical studies were carried out in the liver and kidneys to support the above parameters.ResultsRats injected with CuO-NPs showed higher levels of the above serum marker enzymes, alteration of oxidant–antioxidant balance together with severe pathological alterations in liver and kidney tissues and overexpression of both caspase-3 and nuclear factor kappa B protein (NF-ĸB) associated with upregulation of Bax gene and downregulation of Bcl2 gene in these organs. PJ ameliorated all of the above toxicological parameters.ConclusionPJ was proved to be a potential hepato-renal protective agent against liver and kidney damage induced by CuO-NPs via its antioxidant, anti-inflammatory, and anti-apoptotic effects.

Cardioprotective potential of Spinacia oleracea (Spinach) against isoproterenol-induced myocardial infarction in rats

Context Spinacia oleracea is rich in antioxidant phyto-constituents, termed as the natural antioxidant mixture (NAO). Objective This study investigates the cardioprotective effect of an antioxidant-rich extract of Spinacia oleracea (NAOE) and its phytoconstituent rutin in isoproterenol (ISO)-induced myocardial infarction in rats. Methods Rats were treated with NAOE (400 and 800 mg/kg), rutin (50 mg/kg) and the reference drug gemfibrozil (50 mg/kg) daily for 30 days and were administered ISO (85 mg/kg, s.c) on the last 2 days. Results NAOE treatment attenuated the ISO-elevated levels of serum marker enzymes (AST, LDH and CPK), troponin I, total cholesterol, triglycerides, uric acid, CRP, TNF-α, IL-6 and malondialdehyde. It also restored the ISO-skewed ECG and systolic blood pressure, and the ISO-depleted marker enzymes and endogenous antioxidants in all treated rats. Conclusion It may be concluded that NAOE treatment to ISO-challenged rats exhibited significant cardioprotective effect probably due to the potent antioxidant activity of its NAO.

Nardostachys jatamansi ameliorates doxorubicin induced cardiotoxicity via down regulation oxidative stress and inflammatory markers in rats

Nardostachys jatamansi (family Valerianaceae) is a perennial herb found in Alpine Himalayas. In Ayurveda system of medicine, rhizomes of Nardostachys jatamansi are used as a bitter tonic, stimulant and antispasmodic and to treat epilepsy, hysteria, and convulsions. In the Unani system of medicine Nardostachys jatamansi has been mentioned as hepatotonic, cardiotonic, diuretic and analgesic. In the present study, we have investigated the protective role of alcoholic extract of N. jatamansi on myocardial injury induced by doxorubicin (15 mg/kg body weight, intraperitoneal single dose). Pretreatment for 5 days with ethanolic extract of N. jatamansi (250 mg/kg body weight and 500 mg/kg body weight orally) showed moderate cardioprotective activity as evidenced by significant decline in the elevated levels of serum marker enzymes and lipid peroxide levels with restoration in myocardial endogenous antioxidants levels. Hyperlipidaemia induced by doxorubicin was also inhibited and inflammation markers TNF‐α, IL‐6, and myeloperoxidase [MPO]), were also assessed. Doxorubicin promoted the upregulation of cardiac cytokines (TNF‐α and IL‐6), and MPO activity were significantly down regulated upon ethanolic extract of N. jatamansi pretreatment. Histopathological changes ranging from edema to degenerative changes in cardiac tissue sections were also restored.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Ghrelin prevents cardiac cell apoptosis during cardiac remodelling post experimentally induced myocardial infarction in rats via activation of Raf-MEK1/2-ERK1/2 signalling

Context: Mechanisms by which ghrelin affords its cardioprotection in mammals remained unclear.Objective: To examine if ghrelin confers cardio-protection during cardiac remodelling post-MI by modulating the RAF-1-MEK1/2-ERK1/2 signalling pathway.Materials and methods: Rats were divided into control, sham, sham + ghrelin, myocardial infarction (MI), and MI + ghrelin groups. Ghrelin (100 µg/kg) was administered for 21 days, starting one-day post-MI.Results: Ghrelin enhanced cardiac contractility and the activities of antioxidant enzymes, lowered serum levels of enzyme markers of cardiac dysfunction, and lowered inflammatory mediator levels. Ghrelin increased levels of phospho-Raf-1 (Ser338), phospho-MEK1/2 (Ser217/221), phospho-ERK1/2 (Thr202/Tyr204), and of their downstream target p-BAD (Ser112) and inhibited the cleavage of caspase-3. Concomitantly, ghrelin prevented the increases in the levels of fibrotic markers, including α-smooth muscle actin (α-SMA), metalloproteinase-9 (MPP-9), and type III collagen.Conclusion: Post-MI in rats, ghrelin stimulated Raf-1-MEK1/2-ERK1/2-BAD signalling in the LV infarct areas, accounting for its anti-apoptotic effect, enhancing cardiac function, and inhibiting cardiac fibrosis during cardiac remodelling.

Nonionic surfactant based thymoquinone loaded nanoproniosomal formulation: in vitro physicochemical evaluation and in vivo hepatoprotective efficacy

Context: The present study was carried out to formulate thymoquinone proniosomal formulation (TQP) and evaluate their efficacy in methotrexate (Mtx) induced hepatotoxicity in rats.Objective: The objective of the study was to explore a new therapeutic approach focusing on hepatoprotective activity using thymoquinone proniosomal formulation.Material and methods: TQP was formulated using span60, cholesterol and phospholipid by film hydration technique. The animals were divided into six groups with five animals each receiving different treatments for 7 days. On the 8th day, rats were anesthetized with ether, blood samples were withdrawn, livers were dissected out for biochemical tests and histopathological examinations.Results and discussion: The size of vesicle was found to be in the nanometric range with higher entrapment efficiency. The high entrapment efficiency is probably due to the lipophilic character of TQ. The morphological structure showed the outline and core of the well-identified spherical vesicle, and also displaying the retention of sealed vesicular structure. The release of TQ from developed formulation was found to be significantly higher compared to control. Mtx treated rats showed significant elevation in ALT, AST, ALP and TBARs, whereas, TQP treated group showed significant reduction.Conclusion: The developed formulation (TQP) significantly inhibited the elevated levels of serum marker enzymes and showed improved histopathological deformities.

Protective effects of hepatocyte-specific glycyrrhetic derivatives against carbon tetrachloride-induced liver damage in mice

Glycyrrhetic acid (GA), the main hydrolysate of glycyrrhizic acid extracted from the roots of the Chinese herb Glycyrrhiza glabra, was reported to be accumulated in hepatocytes due to the extensive distribution of GA receptors in liver. A series of hepatocyte-specific derivatives on the basis of anetholtrithione and glycyrrhizic were designed and synthesized. The potential beneficial effect was evaluated in carbon tetrachloride (CCl4)-induced liver injury model. In addition, the hepatoprotective activity of these derivatives was assessed by measuring levels of serum marker enzymes, including serum glutamate oxaloacetate transaminase (GOT), serum glutamate pyruvate transaminase (GPT), alkaline phosphatase (AKP), lactate dehydrogenase (LDH) and the ratio of GSH to GSSG. Gratifyingly, compounds 5a–c (100mg/kg, p.o.) markedly prevented CCl4-induced elevation of levels of serum GPT, GOT. A comparative histopathological study of liver exhibited almost a normal liver lobular architecture and cell structure of the livers, as compared to CCl4-treated group. These findings were confirmed with the histopathological observations, where hepatocyte-specific glycyrrhetic acid derivatives 5a–c were capable of reversing the toxic effects of CCl4 on hepatocytes.

Hepatoprotective and antioxidant effects of fish oil on isoniazid-rifampin induced hepatotoxicity in rats

In the present study hepatoprotective and antioxidant potential of fish oil (cod liver oil) against isoniazid and rifampin combination (INH-RMP)-induced toxicity was evaluated in rats. Administration of (50mg INH+100mg RMP/kg/day, intraperitonially [i.p]) for 14 daysproducedliver injury that was evident from elevated levels of serum marker enzymes, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP), and histopathological changes. The drug treatment caused significant changes in the cellular redox status as reflected by about 75% decrease in the level of serum total antioxidant capacity (TAC), a marked decrease in reduced glutathione (GSH) level, an increased in lipid peroxidation (LPO) in the liver. Fish oil treatment (4ml/kg/day, i.p.) 5–6 hrprior to (INH-RMP) dose, markedlyprevented the rise in serum enzymes levelselicited by the drugs. The histopathological alterations were also improved. Remarkably, there was a complete reversal of the changes in the levels of GSH and LPO, and partial recovery of TAC in the animals receiving fish oil along with (INH-RMP). These observations support the mechanistic role of strong antioxidant property of fish oil in the protection of hepatic injury. This study suggests the importance of fish oil as a hepatoprotective and antioxidant dietary supplement, particularly in the patients receiving anti-tubercular therapy which are at a risk of hepatotoxicity.

Tinospora cordifolia extract attenuates cadmium-induced biochemical and histological alterations in the heart of male Wistar rats

Persistence of cadmium (Cd) in the environment causes serious ecological problems. Tinospora cordifolia is a medicinal herb used in Ayurveda for treating various metabolic disorders and toxic conditions. The present study investigates the protective effect of T. cordifolia stem methanolic extract (TCME) on a heavy metal, Cd-induced cardiotoxicity in male Wistar rats. Male albino Wistar rats were divided into four groups (n=6). The animals after treatment for 28days with Cd and TCME were analysed for biochemical and histological changes in the serum and heart tissues. Cd induced lipid peroxidation and protein carbonylation was significantly reduced by TCME. TCME also reduced the histological alterations induced by Cd treatment in the heart tissues with diminished loss of myocardial fibers. Administration of TCME effectively prevented the altered levels of serum marker enzymes (creatine kinase and lactate dehydrogenase), antioxidants, such as superoxide dismutase, catalase, glutathione, glutathione peroxidase and glutathione-S-transferase, and glycoproteins contents such as hexose, hexoseamine, fucose, and sialic acid by Cd intoxication. TCME also offered protection against the change in levels of Na+K+ATPase, Mg2+ATPase and Ca2+ATPase activities against Cd toxicity. The study suggests TCME as a potent cardioprotective agent against Cd induced toxicity.

Hepatoprotective Effect of Carrot (Daucus carota L.) on Paracetamol Intoxicated Rats

Plant products play a crucial role in the hepatoprotection through its antioxidants property. Therefore, search for modern medicine of plant origin with this property has become a central focus on hepatoprotection today. This study investigated to search a new hepatoprotective agent from natural sources, the methanol extract of nutitional plant, Daucus carota leaves was tested against liver damage of albino rats. Levels of serum marker enzymes i.e. SGOT, SGPT (aminotransferases), ALP (alkaline phosphatase) and TB (total bilirubin) in serum respectively. The histopathological changes of liver sections were also compared with the respective controls. 30% paracetamol induced significant (P<0.05) increase in liver enzymes alongwith the hepatic necrosis and other visible disarrangements in hepatic tissues. Simultaneously, oral treatment with kaempferol (KF) isolated from D. carota plant reversed to all the serum and liver parameters, dose-dependently, in 30% paracetamol treated rats. The biochemical results were also compared with the standard drug i.e. silymarin. These findings indicate the hepatoprotective potential of D. carota fruit against liver damage might be due to the presence of flavonoid like KF constituents.

An Investigation of Hepatoprotective Activity of Methanolic Extract of Ipomoea reniformis on Experimentally Induced Ethanol Hepatotoxicity in Rats

Objective: The present study evaluated the hepatoprotective activity of Methanolic Extract of Ipomoea reniformis (MEIR) in experimentally-induced hepatotoxic rats. Methods: Hepatoprotective activity of MEIR was studied against ethanol (4 g/kg p.o.)-induced hepatotoxicity rats. Silymarin (100 mg/kg p.o.) was used as a standard reference. The following parameters were evaluated; serum biomarkers such as Serum Glutamate Oxaloacetic Transaminase (SGOT), Serum Glutamate Pyruvate Transaminase (SGPT), total and direct bilirubin, Total Protein (TP) and tissue antioxidant levels such as Glutathione (GSH) and Lipid Peroxidation (LPO). Results and conclusion: The control group did not exhibit increase in serum parameters, but ethanol toxicant group showed significant increase in serum parameters such as SGOT, SGPT, bilirubin (total and direct), and LPO, whereas GSH and TP levels were markedly reduced. Silymarin, MEIR low dose (200 mg/kg p.o.) and high dose (400 mg/kg p.o.) treated groups showed significant decrease in SGOT, SGPT, total and direct bilirubin, TB, LPO and increase in GSH and TP levels. Based on the study findings in serum marker enzyme levels and antioxidant parameters, it is concluded that MEIR possesses hepatoprotective activity.

Histopathological and biochemical investigations of protective role of honey in rats with experimental aflatoxicosis.

BackgroundNatural honey (honey) is considered as a part of traditional medicine all over the world. It has both antimicrobial and antioxidant properties, useful in stimulation of wounds and burns healing and gastric ulcers treatment. The aim of this study, for the first time, was to investigate the antioxidant properties and protective role of honey against carcinogen chemical aflatoxin (AF) exposure in rats, which were evaluated by histopathological changes in liver and kidney, measuring level of serum marker enzymes [aspartate aminotransferase (AST), alanin aminotransferase (ALT), gamma glutamil transpeptidase (GGT)], antioxidant defense systems [Reduced glutathione (GSH), glutathione reductase (GR), superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT)], and lipid peroxidation content in liver, erythrocyte, brain, kidney, heart and lungs.MethodsEighteen healthy Sprague–Dawley rats were randomly allocated into three experimental groups: A (Control), B (AF-treated) and C (AF + honey-treated). While rats in group A were fed with a diet without AF, B, and C groups received 25 μg of AF/rat/day, where C group additionally received 1 mL/kg of honey by gavage for 90 days.ResultsAt the end of the 90-day experimental period, we found that the honey supplementation decreased the lipid peroxidation and the levels of enzyme associated with liver damage, increased enzymatic and non-enzymatic antioxidants in the AF + honey-treated rats. Hepatoprotective and nephroprotective effects of honey is further substantiated by showing almost normal histological architecture in AF + honey-treated group, compared to degenerative changes in the liver and kidney of AF-treated rats. Additionally, honey supplementation ameliorated antioxidant defens systems and lipid peroxidation in content in other tissues of AF + honey treated rats.ConclusionThe present study indicates that honey has a hepatoprotective and nephroprotective effect in rats with experimental aflatoxicosis due to its antioxidant activity.

ANTIDIABETIC AND HYPOLIPIDEMIC EFFECT OF METHANOL EXTRACT OF STEREOSPERMUM COLAIS FRUIT IN STREPTOZOTOCIN INDUCED DIABETIC RATS

Objective: To assess the antidiabetic and hypolipidemic properties of Stereospermum colais Fruit. Methods: Acute toxicity test was done to check the toxicity of Stereospermum colais Fruit methanol extract at three dose levels was administered orally to streptozotocin (STZ) (40 mg/kg bw) induced diabetic rats for 15 days. The various parameters were studied including body weight, fasting blood glucose levels, plasma insulin, lipid profile, glycogen content, glycoslylated hemoglobin (HbA1c) and serum marker enzymes levels in normal, treated and diabetic rats. Histochemical analysis of pancreas was also carried out in normal treated and diabetic rats. Results: The treatment group with the extract at three dose levels showed a significant increase in the liver, muscle glycogen and serum insulin level and a significant decrease in fasting blood glucose, glycosylated hemoglobin levels and serum marker enzyme levels. The total cholesterol and serum triglycerides levels were also significantly reduced and the high density lipoprotein level was significantly increased upon treatment with the Stereospermum colais Fruit methanol extract. Histochemical study of pancreas also confirmed the biochemical findings. Acute toxicity studies revealed the non-toxic nature of the Stereospermum colais Fruit methanol extract. Conclusions: The results of the experiments presented here suggest that methanol extract of Stereospermum colais Fruit exerts significant antidiabetic and hypolipidaemic effect in STZ induced diabetic rats. Keywords: Stereospermum colais , Antidiabetic, Hypolipidemic, Fruit, streptozotocin.

Artesunate obliterates experimental hepatocellular carcinoma in rats through suppression of IL-6-JAK-STAT signalling.

Activation of the IL-6 mediated JAK-STAT (Janus associated kinase-signal transducer and activator of transcription) oncogenic signalling plays a major role in hepatocellular carcinoma pathogenesis. The aim of this study is to assess the anti-tumour, anti-proliferative and apoptotic potential of artesunate and its capacity to modulate JAK-STAT pathway in a nitrosodiethylamine mediated experimental hepatocellular carcinoma model. Administration of nitrosodiethylamine (200mg/kg body weight by i.p. Injections) to rats resulted in alterations of liver pathophysiological parameters such as increased relative liver weight, and increased tumour nodule occurrence. It also increased the levels of serum marker enzymes (AST, ALT, ALP, LDH, and γGT) and tumour biomarker (AFP) levels suggestive of its capacity to cause liver tumourigenesis. Additionally, the immunohistochemistry of liver sections pertaining to nitrosodiethylamine administered animals showed increased detection of AgNOR, PCNA, and GST-Pi positive cells suggestive of its capacity to promote liver proliferation associated tumourigenesis. On the contrary, artesunate (25mg/kg bodyweight) supplementation to nitrosodiethylamine administered animals decreased all the above mentioned pathophysiological, biochemical, and immunohistochemistry parameters suggesting its anti-tumour and anti-proliferative potential. Furthermore, immunoblot analysis showed significant up-regulation of IL-6, GP130, JAK-2, STAT-3 (pY705), Bcl-xL, Bcl-2 and simultaneous down-regulation of Caspase-3, PARP and SOCS-3 in nitrosodiethylamine administered animals. Nevertheless, the immunoblot analysis revealed vice-versa on artesunate supplementation to nitrosodiethylamine administered animals, indicating promotion of the feedback loop inhibition mechanism through SOCS3 up-regulation thereby leading to suppression of JAK-STAT signalling. Overall all these findings substantiate that artesunate promotes anti-tumour, anti-proliferation and apoptosis against nitrosodiethylamine mediated hepatocellular carcinoma.