Hepatic Damage In Wistar Rats Research Articles

Protective effects of Alstonia congensis Methanolic extract against CCl4 induced liver damage in Wistar rats

The hepatoprotective potential, phytochemical properties, and in vivo antioxidant activities of methanol extract of Alstonia congensis stem bark were investigated against carbon tetrachloride (CCl4) induced hepatic damage in Wistar rats. The animals (thirty) were separated randomly into five groups of each six rats and kept under standard state (temperature 25± 2) and fed standard rat pellets and water ad libitum. Liver toxicity in rats was achieved by the intraperitoneal injection of a single dose of 3 ml/kg of CCl4 in olive oil, after oral treatment of rats with 200 and 400 mg/kg of methanol extract of A. congensis or silymarin (50 mg/kg/day) for fourteen days. Then the rats were sacrificed by cervical dislocation and blood samples collected through cardiac puncture, while the liver tissues were removed for the biochemical tests. Hepatotoxic changes were measured by evaluation of some hepatic enzymes, markers of oxidative stress, and histopathological examination. The phytochemical analysis of the extracts displayed the presence of Alkaloids, Saponins, Tannins, Terpenoids, Steroids, Anthocyanin, Flavonoids, Anthraquinones, and Phenols. Treatment of rats with methanol extracts of A. congensis resulted in a significant (p < 0.05) decrease in the values of serum alkaline phosphatase (ALP), alanine transaminase (ALT), aspartate aminotransferase (AST), bilirubin, tissue lipid peroxidation (LPO), as well as an increase (p < 0.05) in the levels of total protein, albumin, reduced glutathione (GSH) and the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) to near normal level relative to the CCl4 intoxicated control group (negative control). These observations were buttressed by the histopathological results. Thus, the results revealed that methanol extracts of A. congensis stem bark possess in vivo antioxidant and hepatoprotective effects against CCL4 induced hepatic damage in rats (dose-dependently), which could be attributed to its phytoconstituents.

Ficus glumosa Del. reduces phenylhydrazine-induced hemolytic anaemia and hepatic damage in Wistar rats.

Anemia is a direct or indirect consequence of oxidative stress via free radicals on erythrocytes and subsequently on other tissues like liver. Ficus glumosa constitute a rich pharmacologically compound that can prevent or repair oxidative damage. Therefore, this study seeks to evaluate the effect of F.glumosa on phenylhydrazine-induced hemolytic anemia and hepatic damage in rats. Twenty-four (24) albino Wistar rats were assigned to four (4) experimental groups (n=6) as follows: Group I (non-anemic control) and Group 2 (anemic control) received normal saline, while Group III and IV (test groups) 200 and 400mg/kg of aqueous leaf extract of F.glumosa (ALEFG), respectively. All the groups were treated orally (via a cannula) for seven consecutive days. Intraperitoneal (IP) injection of phenylhydrazine (PHZ) at 40mg/kg for two consecutive days induced hemolytic anemia in group II to IV before treatment. Rats of all groups were anaesthetized and sacrificed 24h after the last treatment. Blood and liver samples were collected for some hematological indices, liver function test, antioxidant parameter and histological analysis. The LD50 of ALEFG was assessed orally in rats and found to be above 5,000mg/kg body weight. Significant (p<0.05) decreases in the level of red blood cell (RBC), hemoglobin (HGB) concentrations and packed cell volume (PCV) by 50% after 2days of PHZ induction, were attenuated by more than 50% after 7days administration of ALEFG at 200 and 400mg/kg. The percentage change in body weight increased significantly (p<0.05) after 7days post PHZ-induced anemia, but those that received oral administration of ALEFG (at 200 and 400mg/kg) for 7days increased significantly (p<0.05) by more than 2%, dose-dependently compared to anemic untreated group. Increased level of serum ALT, AST, ALP and GGT in PHZ-induced anemic animals, were significantly (p<0.05) attenuated in the groups that received oral administration of ALEFG (at 200 and 400mg/kg) for 7days. Decreased level of catalase (CAT) and superoxide dismutase (SOD) activities with concomitant increase in malondialdehyde (MDA) content from PHZ-induced untreated group, were significantly (p<0.05) mitigated in the rats that received oral administration of ALEFG (at 200 and 400mg/kg) for 7days. Histopathological analysis showed that ALEFG could remarkably though not completely mitigated PHZ-induced hepatic damage. Our data suggests that the leaves of F.glumosa contain important antioxidant(s) that could effectively reduce hemolytic anemia and hepatic damage, especially during phenylhydrazine-induced toxicity.

AST/ALT levels, MDA, and liver histopathology ofEchinometra mathaei ethanol extract on paracetamol-induced hepatotoxicity in rats.

Echinometra mathaei was known to have potential antioxidant activities because it contains ofpolyhydroxy-naphthoquinone (echinochrome and spinochromes). The antioxidant properties contributed to the hepatoprotective effect by binding to free radicals compound that causes oxidative stress and necrosis in thehepatocytes. The research aimed to determine the hepatorepair effects of the E.mathaei ethanol extract onhigh-dose paracetamol-induced hepatic damage in Wistar rats. This research used a true experimental method. Thirty white male rats were divided into sixth groups, i.e.,normal control group, group II-VI was induced paracetamol 2,000mg/kg BW for three days. After paracetamol-induced, group III-VI was treated with curcumin 800mg/kg BW, E.mathaei extract 400, 800, and 1,200mg/kg BW for seven days. The hepatorepair parameter was obtained from AST/ALT, MDA tissue levels, and the number of hepatocyte necrosis cells. The data results were analyzed using the ANOVA test, followed by the LSD test to determine the difference between each treatment. The results showed that E.mathaei significantly (p<0.05) decreased the AST levels, MDA levels and the number of hepatocyte necrosis cells at a dose of 800mg/kg BW per orally treatment. The E. mathaei ethanol extract repaired the hepatic damage induced by paracetamol.

Evaluation of Hepatoprotective Activity of Caralluma europaea Stem Extract against CCl4-Induced Hepatic Damage in Wistar Rats.

The present study aims to evaluate the hepatoprotective activity of stem aqueous extract of Caralluma europaea (AECe) on carbon tetrachloride- (CCl4-) induced hepatic damage in Wistar rats. The animals were daily treated with the aqueous extract of C. europaea at a dose of 250 mg/kg body weight for 14 days. CCl4 was injected (1 ml/kg, i.p.) two times, on the 7th and 14th days. At the end of the experimental period, all rats were anesthetized to collect blood for the assessment of biochemical parameters and then sacrificed to collect the liver for weighing. Hepatotoxicity was evaluated by measuring the serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), bilirubin (total and direct), malondialdehyde (MDA), total protein (TP), triglycerides (TG), total cholesterol, very low-density lipoprotein (VLDL-c ), low-density lipoprotein (LDL-c), high-density lipoprotein (HDL-c), urea, creatinine, and uric acid. Based on the results obtained in this study, the administration of C. europaea before exposure to the administration of CCl4 conferred favorable hepatoprotective effect in rats. The treatment with AECe (250 mg/kg) exhibits a significant hepatoprotective effect by ameliorating CCl4-induced alterations of these biochemical parameters. Hence, C. europaea could be a potential medicinal herb that can be used in the future to prevent liver intoxication.

Hepatoprotective, antioxidant and, anti-inflammatory potentials of gallic acid in carbon tetrachloride-induced hepatic damage in Wistar rats.

Gallic acid (GA) is a known phenolic compound with anti-inflammatory, antioxidant, and anti-cancer activities. The objective of this research is to evaluate the preventive role of GA against carbon tetrachloride (CCl4) induced liver fibrosis. Thirty-five (35) male Wistar rats were used in this study and were equally distributed into five groups (7 rats each). All groups were acclimatized for a week, Group I (control) rats were administered distilled water only. Group II rats were induced with a single dose of CCl4 (1.25 mL/kg in olive oil (1:1); IP) to cause hepatic damage, while Groups III, IV, and V, rats were intoxicated with CCl4. After 24 h the rats in groups III, IV, and V were given 50 mg/kg of silymarin, 50 mg/kg of GA, and 100 mg/kg of GA daily for one week respectively. Rats were sacrificed and fasting blood was estimated for biochemical analysis while the liver was excised for molecular studies. Results from this study revealed that GA significantly decreases serum hepatic enzymes, down-regulate the expression of pro-inflammatory cytokines, interleukin 1 beta (IL-1B), interleukin 6 (IL-6), cyclooxygenase 2 (COX 2), and tumor necrosis factor-alpha (TNF α), and up-regulate antioxidant gene expression (superoxide dismutase and catalase). The use of gallic acid as natural antioxidants can be promising in ameliorating liver diseases.

Antioxidant and hepatoprotective potentials of curcuminoid isolates from turmeric (Curcuma longa) rhizome on CCl4-induced hepatic damage in Wistar rats

ABSTRACT The present study examined the protective effects of curcuminoid isolates from Curcuma longa against carbon tetrachloride (CCL4)-induced hepatic injury in rats. The hepatoprotective effect of the crude extract (150, 300 and 600 mg/kg bw) and curcuminoids (75, 150 and 300 mg bw) was evident by significant increases in the serum antioxidative defence capacities (super oxide dismutase, reduced glutathione, catalase) and reduction in biomarker enzymes of liver integrity (aspartate transaminase, alanine transaminase and alkaline phosphatase) in comparison to the results obtained in the CCL4-untreated animals. Some of these parameters were completely restored by pre-treatments with curcuminoids. Similarly, the curcuminoids increases the concentrations of total proteins, albumins and ameliorated histological changes observed in CCL4 injured rats. Therefore, curcuminoid could be considered a novel candidate for the development of new drug against liver diseases.

ANTIOXIDANT AND HEPATOPROTECTIVE EFFECT OF SWERTIA CHIRATA ON HYPOXIA-INDUCED OXIDATIVE STRESS IN WISTAR RATS

Objective: Swertia chirata has been used in traditional and folklore medicine to treat several ailments such as hepatic disorders. However, the mechanistic and experimental justification to its traditional use is lacking. The present study was aimed to investigate the hepatoprotective potential of S. chirata during hypoxia (HYP)-induced hepatic damage in Wistar rats and to determine the underlying mechanism.Methods: Hydroalcoholic extract of S. chirata was prepared using Soxhlet extraction. Animals were divided into six groups (n=5). Animals in the HYP groups were subjected to HYP for 3 days (10% O2) to induce oxidative stress and hepatic damage. 50 and 100 mg/kg extract treatments were provided orally once daily for 7 days after which animals were sacrificed, and biochemical investigations for oxidative stress, liver function tests, and hepatic histopathology were performed.Results: HYP-induced marked oxidative stress as indicated by the significantly elevated mitochondrial ROS generation, lipid peroxidation, glutathione, and depleted catalase levels. Liver function test indicated hepatic damage as the levels of serum glutamic-oxaloacetic transaminase, serum glutamic pyruvic transaminase, and aspartate transaminase were significantly elevated in HYP animals. S. chirata treatment alleviated oxidative stress and improved liver functions in a dose-dependent manner. Liver histopathology confirmed the marked hepatic damage induced by HYP and revealed that S. chirata efficiently rescued liver from hypoxic damage.Conclusion: Hydroalcoholic extract of S. chirata is a potent hepatoprotective intervention which was associated with its potential to alleviate oxidative stress and improve liver functions. Moreover, it could find clinical application as a safer and alternative remedy for liver ailments.

ANTIOXIDANT AND HEPATOPROTECTIVE EFFECT OF SWERTIA CHIRATA ON HYPOXIA-INDUCED OXIDATIVE STRESS IN WISTAR RATS

Objective: Swertia chirata has been used in traditional and folklore medicine to treat several ailments such as hepatic disorders. However, the mechanistic and experimental justification to its traditional use is lacking. The present study was aimed to investigate the hepatoprotective potential of S. chirata during hypoxia (HYP)-induced hepatic damage in Wistar rats and to determine the underlying mechanism.Methods: Hydroalcoholic extract of S. chirata was prepared using Soxhlet extraction. Animals were divided into six groups (n=5). Animals in the HYP groups were subjected to HYP for 3 days (10% O2) to induce oxidative stress and hepatic damage. 50 and 100 mg/kg extract treatments were provided orally once daily for 7 days after which animals were sacrificed, and biochemical investigations for oxidative stress, liver function tests, and hepatic histopathology were performed.Results: HYP-induced marked oxidative stress as indicated by the significantly elevated mitochondrial ROS generation, lipid peroxidation, glutathione, and depleted catalase levels. Liver function test indicated hepatic damage as the levels of serum glutamic-oxaloacetic transaminase, serum glutamic pyruvic transaminase, and aspartate transaminase were significantly elevated in HYP animals. S. chirata treatment alleviated oxidative stress and improved liver functions in a dose-dependent manner. Liver histopathology confirmed the marked hepatic damage induced by HYP and revealed that S. chirata efficiently rescued liver from hypoxic damage.Conclusion: Hydroalcoholic extract of S. chirata is a potent hepatoprotective intervention which was associated with its potential to alleviate oxidative stress and improve liver functions. Moreover, it could find clinical application as a safer and alternative remedy for liver ailments.

Effect of Ethanol Leaf Extract of Spilanthes filicaulis on Liver Indices and Selected Biochemicals on Carbon Tetrachloride Induced Hepatic Damage in Wistar Rats

This study investigated the effect of ethanol leaf extract of Spilanthes filicaulis on liver indices and selected biochemicals on carbon tetrachloride induced hepatic damage in wistar rats. A total of thirty (30) rats comprising of five (5) rats per group (90-130 g), were used for the study. Groups 1-3, served as normal, negative (CCl4 induced 1 mL/kg, 1:1 i.p.) and positive (CCl4 induced and administered with silymarin 50 mg/kg) controls respectively. Groups 4-6 were the extract treated groups administered with 250 mg/Kg bw, 500 mg/Kg bw and 750 mg/Kg bw respectively for 14 days. The results of the liver marker enzymes showed a significant decrease (p 0.05) in all treated groups when compared to the negative control group. Catalase (CAT) and Superoxide Dismutase (SOD) levels were significantly increased (p 0.05) in all treated groups when compared to the negative control. The study showed that the ethanol leaf extract of Spilanthes filicaulis has potential of restoring hepatic liver damage.

Antioxidant activity and hepatoprotective effect of &lt;i&gt;Cichorium intybus&lt;/i&gt; (Kasni) seed extract against carbon tetrachloride-induced liver toxicity in rats

Purpose: To assess the antioxidant and hepatoprotective activity of the aqueous-methanol extract of Cichorium intybus seeds (C. intybus) against carbon tetrachloride (CCl4)-induced liver toxicity in albino Wistar rats.Method: The seed extract of C. intybus was prepared in aqueous methanol (20:80) via Soxhlet solvent extraction process. CCl4 (0.8 mL/kg) was administered to induce hepatic damage in Wistar rats. The seed extract (100, 250 and 500 mg/kg doses) and a 25 mg/kg dose of silymarin (as standard drug) were administered orally to separate groups of albino Wistar rats for 14 days. Blood samples from the rats were analyzed for biochemical markers for hepatic injury. The tissue samples of the rats were subjected to histopathological studies as well as analyzed for liver antioxidants.Results: The results for biochemical markers revealed that the rats treated with the extract (500 mg/kg dose) showed a maximum elevation of catalase (48.90 μmole of H2O2 consumed/min/mg protein), glutothione peroxidase (22.1 mg GSH consumed/min/mg protein), superoxide dismutase (14.2 units/min/mg protein), and a reduction in glutathione (18.1 μmole of GSH/mg protein). Serum biochemical parameters including serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), alkaline phosphate (ALKP), and direct bilirubin were significantly (p < 0.01) increased in the treated groups. Oral administration of different doses of C. intybus seed extract significantly (p < 0.01) protected the hepatic cells from impairment. The biochemical markers and hematological parameters were also normal in extract-treated rats in contrast to the standard (silymarin) and control groups.Conclusion: The results show that C. intybus plant is potential a good natural source of natural hepatoprotective and antioxidants agents.Keywords: Cichorium intybus, Antioxidant, Hepatoprotective Biomarkers, Silymarin, Hematological parameters

Glibenclamide protects against thioacetamide-induced hepatic damage in Wistar rat: investigation on NLRP3, MMP-2, and stellate cell activation.

Glibenclamide (GLB), most widely used in the treatment of type II diabetes mellitus, inhibits K+ATP channel in pancreatic-β cells and releases insulin, while thioacetamide (TAA) is a well-known hepatotoxicant and most recommended for the induction of acute and chronic liver disease. The purpose of this study was to evaluate the hepatoprotective potential of GLB against TAA-induced hepatic damage in Wistar rats. TAA (200mg/kg, ip, twice weekly) and GLB (1.25, 2.5, and 5mg/kg/day, po) were administered for 6 consecutive weeks. Different biochemical, DNA damage, histopathological, TEM, immunohistochemical, and western blotting parameters were evaluated. GLB treatment has no effects on the TAA-induced significant decrease in body and liver weights. TAA treatment significantly increased liver index and treatment with GLB has no effect the same. TAA treatment altered the liver morphology, whereas treatment with GLB normalized the alteration in morphology. Further, significant increase in oxidative stress, apoptosis, and DNA damage was found in TAA-treated animals and GLB treatment significantly reduced these effects. TAA-induced plasma transaminases and serum ALP levels were significantly restored by GLB. Furthermore, histopathological findings showed the presence of lymphocyte infiltration, collagen deposition, bridging fibrosis, degeneration of portal triad, and necrosis in TAA-treated animals and GLB intervention significantly reduced the same. TEM images revealed that GLB significantly normalized the hepatic stellate cell morphology as well as restored the number of lipid droplets. GLB treatment significantly downregulated the expressions of TGF-β1, α-SMA, NLRP3, ASC, caspase-1, and IL-1β, and upregulated MMP-2 and catalase against TAA-induced liver damage. The outcomes of the present study confirmed that GLB ameliorated the liver damage induced by TAA.

Toxic effects of imidacloprid combined with arsenic: Oxidative stress in rat liver.

Imidacloprid (IMI), a newer neonicotinoid insecticide, induces oxidative insult to hepatocytes due to the formation of reactive metabolites during hepatic metabolism. The present study aimed to determine the potentiating effect of arsenic (As) on IMI-induced hepatic damage in Wistar rats. Rats, randomly divided into eight groups with six in each, were subjected to daily oral administration for 28 days. Group I served as control; group II received IMI at the dose rate of 16.9 mg/kg body weight; groups III, IV, and V received As at the dose rate of 50, 100, and 150 ppb, respectively, in drinking water; groups VI, VII, and VIII received both IMI (16.9 mg/kg) and As in drinking water at the rate of 50, 100, and 150 ppb, respectively. Repeated oral administration of IMI or As resulted in significant ( p < 0.05) elevation of plasma phosphatases, transferases, hepatic malondialdehyde, and advanced oxidation protein product levels, but significantly ( p < 0.05) decreased levels of total proteins, thiols, and activities of antioxidant enzymes that indicate oxidation-induced hepatotoxicity. These findings were further corroborated by histological alterations in hepatic tissue of IMI or As-administered rats. The coadministration of both IMI and As in rats produced more severe alterations in these parameters in hepatic tissue. Reduced antioxidant indices and increased hepatic damage biomarkers with pronounced histopathological alterations in hepatic tissue after combined exposure to toxicants indicate potentiating toxic effect of As on IMI-induced hepatotoxicity.

Ethyl acetate fraction of Pteris vittata L. alleviates 2-acetylaminofluorene induced hepatic alterations in male Wistar rats.

Pteris vittata L. commonly called 'Brake Fern' possesses some interesting medicinal properties but its chemopreventive potential largely remains unexplored. Therefore, this study was designed to explore the chemopreventive efficacy of P. vittata L. ethyl acetate fraction (PVEA) against 2-acetylaminofluorene (2-AAF) induced liver toxicity in Wistar rats. Antioxidant activity of PVEA was evaluated using various in vitro antioxidant assays. The protective effects of PVEA were evaluated against 2-acetylaminofluorene (2-AAF) induced hepatic damage in Wistar rats. p53 expression in liver tissue was checked using immunohistochemical staining. Phytochemical composition of PVEA was determined using high performance liquid chromatography (HPLC). PVEA showed promising radical scavenging activity with an EC50 (concentration of a drug that gives half-maximal response) of 41.18μg/ml in DPPH assay, 26.99μg/ml in site specific deoxyribose degradation assay, 13.43μg/ml in non site specific deoxyribose degradation assay and 21.88μg/ml in superoxide anion scavenging assay. Three different doses of PVEA 100, 200 and 400mg/kg body weight (b.w.) followed by administration of 2-AAF (50mg/kg b.w. i.p.) for five consecutive days induced significant changes in activity of liver marker enzymes, thiobarbituric acid reactive substances, lipid hydroperoxides, reduced glutathione content and phase I and II enzymes. Activity of hepatic enzymes and normal hepatic architecture was restored following PVEA treatment. PVEA modulated the expression of p53 in liver tissue as compared to 2-AAF treated group. HPLC analysis of the fraction revealed the abundance of epicatechin (20.809ppm) and umbelliferone (22.308ppm) as major polyphenols. The present study highlights the potentiality of P. vittata in cancer chemoprevention which warrants further investigations.

Hepatoprotective effect of Balanites aegyptiaca (L.) Delile leaves against carbon tetrachloride-induced hepatic damage in rats

Methanolic extract of Balanites aegyptiaca ( L. ) Delile (leaves), was evaluated for its hepatoprotective activity against carbon tetrachloride (CCl 4 )-induced hepatic damage in Wistar rats; by measuring levels of serum marker enzymes like serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), alkaline phosphatase (ALP) and total bilirubin. Histological studies were also carried out to support our hypothesis. Administration of the extract (200 and 400 mg/kg) orally markedly prevented CCl 4 -induced elevation of serum GPT, GOT, ALP and total bilirubin levels. A comparative histopathological study of liver in treated groups exhibited similarity to normal tissue architecture, compared to CCl 4 -treated group.

Glucose-6-phosphate Dehydrogenase Activity During Nʹ-nitrosodiethylamine-induced Hepatic Damage

Glucose-6-phosphate dehydrogenase (G6PD), a key regulatory enzyme of the pentose phosphate pathway, catalyses the first rate-limiting reaction to produce ribose-5-phosphate for nucleic acid synthesis and NADPH to use in reductive biosynthesis. The available studies indicate an antioxidant role for G6PD and variation in its levels as a result of cellular insult. In this study, the activity of G6PD was monitored during Nʹ-nitrosodiethylamine (NDEA)-induced hepatic damage in Wistar rats. NDEA generates hepatotoxicity and possesses mutagenic effects. To induce hepatic damage, NDEA was administered at doses of 100mgkg−1body weightweek−1 (i.p.) for 14days. The animals of the control and treated groups were sacrificed each week. The extent of liver damage was ensured by LFT biomarkers, such as transaminases, ALP, bilirubin and the hepato-somatic index (HSI) along with histopathological observations of H&E and Masson's trichrome stained liver specimens. The results of the present study show that at the selected doses, NDEA significantly elevates LFT proteins and bilirubin and damages the lobular architecture in a dose-dependent manner. Software analysis of zymograms indicates maximum activity of the hepatic G6PD levels in day-14 NDEA-treated animals. Our spectrophotometry data further support the above findings on hepatic G6PD levels and demonstrate an approximately 1.63× and 1.66× fold increase in day-7 and day-14 NDEA intoxicated animals (P<0.05). It is concluded that elevation in the G6PD activity is apparently the consequence of NDEA-induced intoxication or oxidative stress, leading to hepatic damage to provide sufficient NADPH for microsomal detoxification and ribose-5-phosphate for DNA synthesis and repair, respectively, to maintain the cellular redox status.

Hepatoprotective effect of Rhodiola imbricata rhizome against paracetamol-induced liver toxicity in rats

Rhodiola imbricata is a perennial herb of the family Crassulaceae, which has significant traditional usage as medicine and is also known to biosynthesize phytochemicals such as flavonoids, coumarins and phenyl glycosides. The present investigation was aimed to estimate the hepatoprotective activity of R. imbricata rhizome acetone extract against paracetamol (2g/kg) induced liver toxicity. Paracetamol was administered to induce hepatic damage in Wistar rats. 200 and 400mg/kg doses of rhizome acetone extract and silymarin (25mg/kg) were used as treatment groups. The blood samples were analyzed for biochemical markers of hepatic injury and tissue samples were subjected for estimation of liver antioxidants and histopathological studies. Analysis of the extract treated rats (400mg/kg) showed an elevation of superoxide dismutase (0.326units/min/mg protein), catalase (185.03μmole of H2O2 consumed/min/mg protein), glutothione peroxidase (19.26mg GSH consumed/min/mg protein) and reduced glutathione (16.2μmole of GSH/mg protein). Moreover, the biochemical parameters in serum like alkaline phosphatase, serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT) and lipid profiles were also improved in treated groups compared to the control. The oral administration of different doses of rhizome acetone extract significantly protected the hepatic cells from damage. The hematological and biochemical parameters were also normal in extract treated rats compared to the control and standard (silymarin) groups. The HPLC analysis revealed the presence of some important phenolic compounds which could be responsible for the hepatoprotective activity. This study proved that R. imbricata could be taken as a good natural source of the hepatoprotective agent.

Protective Effect ofAcacia nilotica(L.) against Acetaminophen-Induced Hepatocellular Damage in Wistar Rats

The potential biological functions of A. nilotica have long been described in traditional system of medicine. However, the protective effect of A. nilotica on acetaminophen-induced hepatotoxicity is still unknown. The present study attempted to investigate the protective effect of A. nilotica against acetaminophen-induced hepatic damage in Wistar rats. The biochemical liver functional tests Alanine transaminase (ALT), Aspartate transaminase (AST), Alkaline phosphatase (ALP), total bilirubin, total protein, oxidative stress test (Lipid peroxidation), antioxidant parameter glutathione (GSH), and histopathological changes were examined. Our results show that the pretreatment with A. nilotica (250 mg/kg·bw) orally revealed attenuation of serum activities of ALT, AST, ALP, liver weight, and total bilirubin levels that were enhanced by administration of acetaminophen. Further, pretreatment with extract elevated the total protein and GSH level and decreased the level of LPO. Histopathological analysis confirmed the alleviation of liver damage and reduced lesions caused by acetaminophen. The present study undoubtedly provides a proof that hepatoprotective action of A. nilotica extract may rely on its effect on reducing the oxidative stress in acetaminophen-induced hepatic damage in rat model.

Liver Protective Activity of the Methanol Extract of Crinum jagus Bulb against Acetaminophen-induced Hepatic Damage in Wistar Rats

Liver Protective Activity of the Methanol Extract of Crinum jagus Bulb against Acetaminophen-induced Hepatic Damage in Wistar Rats

Effect of Smilax zeylanica roots and rhizomes in paracetamol induced hepatotoxicity

Smilax zeylanica L.(Smilacaceae) is a climbing shrub with woody prickly stems. This study evaluated the hepatoprotective effect of S. zeylanica against paracetamol induced hepatotoxicity in Wistar rats. The protective effects of the methanol extract (200 and 400 mg/kg) of root and rhizome of S. zeylanica were studied on paracetamol induced (1 g/kg) hepatic damage in Wistar rats by estimating the serum levels of AST, ALT, alkaline phosphatase (ALP), total proteins, total bilirubin and albumin. Sections of liver were observed for histopathological changes in liver architecture. Rats were protected from the hepatotoxic action of paracetamol as evidenced by the significant reduction in the elevated serum levels of ALT (P<0.001), AST (P< 0.01, P< 0.001), ALP (P<0.05, P< 0.001), total bilirubin (P< 0.05) and an increased level of total protein (P< 0.05) and albumin (P< 0.05, P<0.01) with a significant reduction in liver weight (P<0.001), when compared with the paracetamol control. Silymarin (100 mg/kg) was used as the standard. The biochemical observations were supplemented by the histopathological studies on the liver sections of different groups. The methanol extract of S. zeylanica was found to alter the damage caused to hepatocytes by paracetamol and prevent the leakage of vital serum markers, which confirmed the hepatoprotective effect of this plant.

Hepatoprotective studies onUtleria salicifoliaBedd. Ex. Hook. f.

The present study was aimed at assessing the hepatoprotective activity of the ethanolic extract of Utleria salicifolia rhizome (US) against paracetamol (APAP)/carbon tetrachloride (CCl4) - induced hepatic damage in Wistar rats. US extract (100 and 200 mg/kg) and standard, silymarin (100 mg/kg, p.o) were tested for their anti - hepatotoxic activity against APAP/CCl4. The treatments substantially elevated serum marker enzymes such as glutamate pyruvate transaminase (SGPT), glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase (SAKP) and bilirubin (SB). These values were restored towards normalization in rats pretreated with US (100 and 200 mg/kg), before the hepatotoxin administration. The biochemical observations were supplemented by histopathological examination of liver sections. US also showed significant free radical scavenging activity in vitro. The results justify the use of U. salicifolia rhizome as a hepatoprotective agent. The results of the study indicate that US rhizome possesses potential hepatoprotective activity against APAP/CCl4 induced liver toxicity, which may be attributed to its free radical scavenging potential, due to the active constituents present in it.