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Hepatoprotective Activity (hepatoprotective + activity)
Selected AbstractsHepatoprotective Activity of Polyherbal Formulation (Normeta®) in Oxidative Stress Induced by Alcohol, Polyunsaturated Fatty Acids and Iron in RatsBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 3 2009Shilpa N. Patere The present study was carried out to evaluate the effects of oral treatment with polyherbal formulation Normeta® (2 ml and 4 ml/kg) on hepatic damage induced by alcohol 10,30% (blood alcohol was maintained at levels between 150 and 350 mg/dl), thermally oxidized oil (polyunsaturated fatty acids) (15% of diet) and carbonyl iron (1.5,2% of diet) for 30 days in rats. In vitro studies with 1, 1-Diphenyl, 2-Picrylhydrazyl (DPPH), Nitric oxide and Ferric chloride (Fe+3 ions) showed that Normeta® possesses antioxidant and metal chelating activity. Alcohol, polyunsaturated fatty acids and iron feeding produced an increase in serum levels of iron, serum glutamate pyruvate transaminase and decrease in serum proteins. It was also associated with elevated lipid peroxidation (thiobarbituric acid reactive substances) and disruption of antioxidant defence mechanism in liver, decreased body weight and increased liver to body weight ratio. Oral administration of Normeta® along with alcohol, polyunsaturated fatty acids and iron decreased the serum iron, serum glutamate pyruvate transaminase levels and increased serum protein levels. The levels of liver thiobarbituric acid reactive substances were decreased and the activities of antioxidant enzymes superoxide dismutase and catalase were increased. Improvement in body weight and liver to body weight ratio was also observed. The effects of Normeta® on physico-metabolic parameters were comparable with silymarin. This indicates that Normeta® has favourable effect in bringing down the severity of hepatotoxicity. [source] Hepatoprotective activity of picroliv, curcumin and ellagic acid compared to silymarin on paracetamol induced liver toxicity in miceFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 6 2009C. Girish Abstract Oxidative stress is implicated as a common pathologic mechanism contributing to the initiation and progression of hepatic damage in a variety of liver disorders. Present study attempts to evaluate the hepatoprotective activity of picroliv, curcumin and ellagic acid in comparison to silymarin using paracetamol (PCM) induced acute liver damage. Hepatotoxicity was induced by administering a single oral dose of PCM (500 mg/kg) and was assessed by quantifying the serum enzyme activities, phenobarbitone induced sleeping time and histopathological analysis of liver tissues. The antioxidant parameters, malondialdehyde (MDA), reduced glutathione (GSH) and catalase of the liver tissue were also assessed. The herbal drugs were administered for 7 days by oral route at 50 and 100 mg/kg. PCM induced hepatic damage was manifested by a significant increase in the activities of marker enzymes (alanine transaminase, aspartate transaminase and alkaline phosphatase) in serum and MDA level in liver. There was also a significant decrease in activity of GSH and catalase levels. The histopathological examination on toxic models revealed centrizonal necrosis and fatty changes. Pretreatment of mice with picroliv, curcumin and ellagic acid reversed these altered parameters towards normal values, which were compared with silymarin. The normalization of phenobarbitone induced sleeping time suggests the restoration of liver cytochrome P450 enzymes. This study supports the use of these active phytochemicals against toxic liver injury, which may act by preventing the lipid peroxidation and augmenting the antioxidant defense system or regeneration of hepatocytes. These active phytochemicals may be developed as drugs for the treatment of liver diseases. [source] Hepatoprotective activity of Terminalia catappa L. leaves and its two triterpenoidsJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 11 2004Jing Gao The aim of this study was to evaluate the effect of the chloroform extract of Terminalia catappa L. leaves (TCCE) on carbon tetrachloride (CCI4)-induced acute liver damage and D-galactosamine (D-GaIN)-induced hepatocyte injury. Moreover, the effects of ursolic acid and asiatic acid, two isolated components of TCCE, on mitochondria and free radicals were investigated to determine the mechanism underlying the action of TCCE on hepatotoxicity. In the acute hepatic damage test, remarkable rises in the activity of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) (5.7- and 2.0-fold) induced by CCI4 were reversed and significant morphological changes were lessened with pre-treatment with 50 and 100 mg kg,1 TCCE. In the hepatocyte injury experiment, the increases in ALT and AST levels (1.9- and 2.1-fold) in the medium of primary cultured hepatocytes induced by D-GaIN were blocked by pre-treatment with 0.05, 0.1, 0.5 gL,1 TCCE. In addition, Ca2+ -induced mitochondrial swelling was dose-dependently inhibited by 50,500 ,m ursolic acid and asiatic acid. Both ursolic acid and asiatic acid, at concentrations ranging from 50 to 500 ,m, showed dose-dependent superoxide anion and hydroxyl radical scavenging activity. It can be concluded that TCCE has hepatoprotective activity and the mechanism is related to protection of liver mitochondria and the scavenging action on free radicals. [source] Hepatoprotective activity of aqueous,methanol extract of Artemisia vulgarisPHYTOTHERAPY RESEARCH, Issue 2 2005Anwarul Hassan Gilani Abstract The effect of a crude extract of the aerial parts of Artemisia vulgaris (Av.Cr) was investigated against D -galactosamine (D -GalN) and lipopolysaccharide (LPS) induced hepatitis in mice. Co-administration of D -GalN (700 mg[sol ]kg) and LPS (1 µg[sol ]kg) significantly (p < 0.05) raised the plasma levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in mice in the toxin group compared with the values in the control group. Pre-treatment of mice with different doses of Av.Cr (150,600 mg[sol ]kg) significantly (p < 0.05) reduced the toxin-induced rise in plasma ALT and AST. The hepatoprotective effect was further verified by histopathology of the liver, which showed improved architecture, absence of parenchyma congestion, decreased cellular swelling and apoptotic cells, compared with the findings in the toxin group of animals. These findings scientifically validated the traditional use of Artemisia vulgaris for various liver disorders. Copyright © 2005 John Wiley & Sons, Ltd. [source] ,-Glucuronidase inhibitor tectorigenin isolated from the flower of Pueraria thunbergiana protects carbon tetrachloride-induced liver injuryLIVER INTERNATIONAL, Issue 4 2003Hae-Woong Lee Abstract Background/Aim: To understand the relationship between the fluctuation in serum ,-glucuronidase and hepatotoxicity, an inhibitor of ,-glucuronidase was isolated from the flowers of Pueraria thunbergiana and its hepatoprotective activity was measured. Method: Tectorigenin was isolated from the flowers of pueria thunbergiana as an inhibitor of ,-glucuronidase, and serum ALT, AST and biological parameters as markers for its hepatoprotective activity were measured on CCl4 -induced liver injury in mice. The relationship between serum ,-glucuronidase and hepatoprotective activities in mice was measured. Results: When tectorigenin at a dose of 100 mg/kg was intraperitoneally administered on CCl4 -induced liver injury in mice, it significantly inhibited the increase of plasma ALT, AST and LDH activities. The inhibitory effect of tectorigenin is much more potent than that of dimethyl diphenyl bicarboxylate (DDB), which has been used as a commercial hepatoprotective agent. When tectoridin transformed to tectorigenin by intestinal bacteria was orally administered to mice, it showed hepatoprotective activity. However, when tectoridin was intraperitoneally administrated to mice, it did not exhibit hepatoprotective activity. Moreover, orally administered tectoridin not only inhibited ,-glucuronidase but also increased GSH content and GST activity on CCl4 -induced hepatotoxicity of mice. Conclusion: We insist that an inhibitor of ,-glucuronidase tectorigenin may be hepatoprotective and tectoridin should be a prodrug transformed to tectorigenin. [source] Analgesic and hepatotoxic effects of Ononis spinosa L.PHYTOTHERAPY RESEARCH, Issue 6 2006Betül Sever Yőlmaz Abstract The present study investigated the analgesic and hepatoprotective activities of a water extract of Ononis spinosa L. (OS) in mice. Analgesic activity was based on the pain thresholds measured with the tail-flick test before administration at 30, 90 and 150 min. The results were analysed with one-way variance analysis. The extract of Ononis spinosa showed analgesic activity equivalent to aspirin at 30 and 90 min and even higher than aspirin with the 50 mg/kg dose. At a dose of 100 mg/kg OS showed an analgesic effect equivalent to aspirin at all time points. The hepatoprotective influence of OS on carbon tetrachloride (CCl4)-induced acute liver toxicity was also studied. The extract had no significant effect on the increased levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and bilirubin in CCl4 treated animals (p > 0.05). Thus, the results reveal that the extract of OS had no hepatoprotective effect on CCl4 -induced acute liver toxicity. Copyright © 2006 John Wiley & Sons, Ltd. [source] Hepatoprotective and antioxidant effects of Alnus japonica extracts on acetaminophen-induced hepatotoxicity in ratsPHYTOTHERAPY RESEARCH, Issue 12 2004Sang Tae Kim Abstract The stem bark of the Betulaceae plant Alnus japonica, which is indigenous to Korea, has been used as a popular folk medicine for hepatitis and cancer. In this study, the antioxidant activity of the crude extract and the hepatoprotective activities on acetaminophen (AAP)-induced toxicity in the rat liver were evaluated. We investigated the effect of the methanol (AJM) and solvent fracton of the stem bark of Alnus japonica (AJ) on AAP-induced hepatotoxicity in rats. In rat hepatocyte culture, pretreatment with AJM (50, 100, 150 and 200 µg[sol ]ml) significantly decreased the cytotoxicity of AAP in a dose-dependent manner. The pretreated with EtOAc and BuOH fraction led to an increase in free radical scavenging activity and a decrease in inhibition of lipid peroxidation, both superoxide dismutase and catalase prevent the hepatotoxicity by AAP in the treatment of A. japonica fraction. We conclude that AJ is an important antioxidant in AAP-induced live hepatotoxicity and that extract of AJM plays a hepatoprotective effects in the against AAP-induced cytotoxicity in cultured rat hepatocytes in vitro. Pending more evaluation for safety and efficacy, AJ can potentially be used in mitigating AAP-induced hepatotoxicity. Copyright © 2004 John Wiley & Sons, Ltd. [source] Hepatoprotective and antioxidant activities of Tetracera loureiriPHYTOTHERAPY RESEARCH, Issue 7 2003Veerapol Kukongviriyapan Abstract Tetracera loureiri is one of the most valued herbs in Thai traditional medicine. In this study, we describe its in vitro and in vivo antioxidant and hepatoprotective activities. The ethanol extract of T. loureiri possessed potent antioxidant and strong free radical scavenging properties assayed using ferric reducing antioxidant power (FRAP) and 2,2-diphenyl-1-picrylhydrazyl (DPPH), respectively. The cytoprotective effects of T. loureiri were demonstrated in ethanolic extracts of freshly isolated rat hepatocytes against the chemical toxicants paracetamol and tertiary-butylhydroperoxide. The cells pretreated with the extract maintained the GSH/GSSG ratio and suppressed lipid peroxidation in a dose dependent manner. Pretreating rats with the ethanol extract orally, one hour prior to intraperitoneal injection of toxic doses of paracetamol, signi,cantly prevented elevations of plasma ALT and AST. These results suggest that T. loureiri may be of potential therapeutic value in some liver disorders. Copyright © 2003 John Wiley & Sons, Ltd. [source] Hepatoprotective activity of picroliv, curcumin and ellagic acid compared to silymarin on paracetamol induced liver toxicity in miceFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 6 2009C. Girish Abstract Oxidative stress is implicated as a common pathologic mechanism contributing to the initiation and progression of hepatic damage in a variety of liver disorders. Present study attempts to evaluate the hepatoprotective activity of picroliv, curcumin and ellagic acid in comparison to silymarin using paracetamol (PCM) induced acute liver damage. Hepatotoxicity was induced by administering a single oral dose of PCM (500 mg/kg) and was assessed by quantifying the serum enzyme activities, phenobarbitone induced sleeping time and histopathological analysis of liver tissues. The antioxidant parameters, malondialdehyde (MDA), reduced glutathione (GSH) and catalase of the liver tissue were also assessed. The herbal drugs were administered for 7 days by oral route at 50 and 100 mg/kg. PCM induced hepatic damage was manifested by a significant increase in the activities of marker enzymes (alanine transaminase, aspartate transaminase and alkaline phosphatase) in serum and MDA level in liver. There was also a significant decrease in activity of GSH and catalase levels. The histopathological examination on toxic models revealed centrizonal necrosis and fatty changes. Pretreatment of mice with picroliv, curcumin and ellagic acid reversed these altered parameters towards normal values, which were compared with silymarin. The normalization of phenobarbitone induced sleeping time suggests the restoration of liver cytochrome P450 enzymes. This study supports the use of these active phytochemicals against toxic liver injury, which may act by preventing the lipid peroxidation and augmenting the antioxidant defense system or regeneration of hepatocytes. These active phytochemicals may be developed as drugs for the treatment of liver diseases. [source] Selective CB1 cannabinoid receptor antagonist, SR141716A, attenuates liver injury induced by Concanavalin AHEPATOLOGY RESEARCH, Issue 4 2009Midori Kojima Aim:, The aim of this study was to investigate the hepatoprotective activity of a selective cannabinoid receptor 1 (CB1) antagonist, SR141716A, in a Concanavalin A (Con A)-induced mouse liver injury model and to determine whether SR141716A has an effect on the production of inflammatory cytokines and chemokines induced by Con A. Results:, Injection of Con A (20 mg/kg) to mice developed hepatitis determined by plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) elevation and necrosis in the liver. Pretreatment with SR141716A (30 mg/kg) significantly reduced plasma AST and ALT level, protected against necrosis in the liver, and significantly reduced plasma cytokine and chemokine levels, including TNF,, IFN-,, CXCL9, MIP1-,, and IL-10 and no change decreased in IL-4. Conclusions:, The selective CB1 antagonist, SR141716A, exerts a hepatoprotective effect on Con A-induced liver injury in mice by attenuating the increase in cytokine and chemokine levels and inhibiting hepatocyte injury. These findings raise the possibility of using CB1 antagonists as anti-inflammatory drugs for treating hepatitis as well as other inflammatory diseases. [source] Structure-hepatoprotective activity relationship study of sesquiterpene lactones: A QSAR analysisINTERNATIONAL JOURNAL OF QUANTUM CHEMISTRY, Issue 1 2009Yuliya Paukku Abstract This study has been carried out using quantitative structure-activity relationship analysis (QSAR) for 22 sesquiterpene lactones to correlate and predict their hepatoprotective activity. Sesquiterpenoids, the largest class of terpenoids, are a widespread group of substances occurring in various plant organisms. QSAR analysis was carried out using methods such as genetic algorithm for variables selection among generated and calculated descriptors and multiple linear regression analysis. Quantum-chemical calculations have been performed by density functional theory at B3LYP/6-311G(d, p) level for evaluation of electronic properties using reference geometries optimized by semi-empirical AM1 approach. Three models describing hepatoprotective activity values for series of sesquiterpene lactones are proposed. The obtained models are useful for description of sesquiterpene lactones hepatoprotective activity and can be used to estimate the hepatoprotective activity of new substituted sesquiterpene lactones. The models obtained in our study show not only statistical significance, but also good predictive ability. The estimated predictive ability (r) of these models lies within 0.942,0.969. © 2008 Wiley Periodicals, Inc. Int J Quantum Chem, 2009 [source] Structure,hepatoprotective activity relationship of 3,4-dihydroxycinnamic acid (caffeic acid) derivativesJOURNAL OF APPLIED TOXICOLOGY, Issue 6 2001V. Pérez-Alvarez Abstract 3,4-Dihydroxycinnamic acid (caffeic acid, CAF) is a natural product containing a catechol group with an ,,,-unsaturated carboxylic acid chain that has shown hepatoprotective properties. The aim of this work was to determine the importance of the 4-hydroxy, 3-hydroxy, 3,4-dihydroxy substituents and the double bond moiety on the hepatic pharmacological effects of the molecule. We compared the ability of the caffeic, 4-hydroxycinnamic, 3-hydroxycinnamic, cinnamic and 3,4-dihydroxyhydrocinnamic (a caffeic acid analogue without the double bond) acids at a dose of 50 mg kg,1, p.o., to reduce the liver damage produced by CCl4 (4 g kg,1, p.o.) intoxication in the rat. Cinnamic acid, the non-hydroxylated analogue, only modestly protected the experimental animals challenged with CCl4, suggesting that hydroxyl groups participate in the pharmacological properties of CAF. The 3,4-dihydroxyhydrocinnamic derivative did not show any significant differences when compared with the CAF effect in this model, suggesting that the double bond does not account for the liver pharmacological properties of CAF. In contrast, the 4-hydroxy substituent seems to be very important for hepatoprotective activity because the 4-hydroxy analogue improved almost every hepatic injury marker altered by CCl4, and in a better way than CAF did. Copyright © 2001 John Wiley & Sons, Ltd. [source] Carotenoid lutein protects rats from paracetamol-, carbon tetrachloride- and ethanol-induced hepatic damageJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 8 2010Edakkadath R. Sindhu Abstract Objectives, Carotenoids are a class of natural fat-soluble pigments that are found in many fruits and vegetables. Consumption of a diet rich in carotenoids has been epidemiologically correlated with a lower risk for several diseases. In the present study the carotenoid lutein (3,3,-dihydroxy- ,,, -carotene) was evaluated for its hepatoprotective activity in rats. Methods, Paracetamol, 20% ethanol and carbon tetrachloride were used to induce liver toxicity. Key findings, Levels of serum glutamate oxaloacetate transaminase, serum glutamate pyruvate transaminase and alkaline phosphatases, which were increased in the serum, were found to be significantly reduced by the treatment of lutein in a dose-dependent manner, indicating that lutein may reduce the hepatotoxicity induced by these agents. Serum bilirubin was also significantly lower in lutein-treated groups compared with control. Increased lipid peroxidation, conjugated diene and hydroperoxides in the liver tissue produced by the administration of paracetamol were found to be reduced in the lutein-treated groups. Levels of antioxidant enzymes, like superoxide dismutase, catalase, glutathione peroxidase and glutathione, were found to be increased in lutein-treated groups compared with control group during alcohol- and CCl4 -induced liver toxicity. Hydroxyproline, which is an indicator of fibrosis in liver tissue, was high in the ethanol-treated control group. Hydroxyproline levels were decreased by simultaneous lutein administration. Conclusions, Histopathological evidence confirmed the protection offered by lutein from the tissue damage caused by hepatotoxins. The hepatoprotective action may be due to lutein's ability to scavenge reactive oxygen radicals. [source] Protective effect of total flavonoids from Bidens bipinnata L. against carbon tetrachloride-induced liver injury in miceJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 7 2007Ming-mei Zhong Bidens bipinnata L. is well known in China as a traditional Chinese medicine. This study was designed to evaluate the hepatoprotective activity of the total flavonoids of B. bipinnata L. (TFB) against carbon tetrachloride (CCI4)-induced acute liver injury in mice and to determine its mechanism of action. Oral administration of TFB at doses of 50, 100 and 200 mg kg,1 for 7 days significantly reduced the elevated relative values of liver weight, serum transaminases (alanine aminotransferase and aspartate aminotransferase) and the hepatic morphologic changes induced by CCl4 in mice. In addition, TFB markedly inhibited CCl4 -induced lipid peroxidation and enhanced the activity of the antioxidant enzymes superoxide dismutase and glutathione peroxidase. Moreover, pretreatment with TFB suppressed nitric oxide production and nuclear factor- kB activation in CCl4 -treated mice. The results suggest that TFB has significant hepatoprotective activity and its mechanism is related, at least in part, to its antioxidant properties. Further research is required to investigate the detailed mechanism of the protective effect of TFB on acute liver injury. [source] Hepatoprotective activity of Terminalia catappa L. leaves and its two triterpenoidsJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 11 2004Jing Gao The aim of this study was to evaluate the effect of the chloroform extract of Terminalia catappa L. leaves (TCCE) on carbon tetrachloride (CCI4)-induced acute liver damage and D-galactosamine (D-GaIN)-induced hepatocyte injury. Moreover, the effects of ursolic acid and asiatic acid, two isolated components of TCCE, on mitochondria and free radicals were investigated to determine the mechanism underlying the action of TCCE on hepatotoxicity. In the acute hepatic damage test, remarkable rises in the activity of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) (5.7- and 2.0-fold) induced by CCI4 were reversed and significant morphological changes were lessened with pre-treatment with 50 and 100 mg kg,1 TCCE. In the hepatocyte injury experiment, the increases in ALT and AST levels (1.9- and 2.1-fold) in the medium of primary cultured hepatocytes induced by D-GaIN were blocked by pre-treatment with 0.05, 0.1, 0.5 gL,1 TCCE. In addition, Ca2+ -induced mitochondrial swelling was dose-dependently inhibited by 50,500 ,m ursolic acid and asiatic acid. Both ursolic acid and asiatic acid, at concentrations ranging from 50 to 500 ,m, showed dose-dependent superoxide anion and hydroxyl radical scavenging activity. It can be concluded that TCCE has hepatoprotective activity and the mechanism is related to protection of liver mitochondria and the scavenging action on free radicals. [source] ,-Glucuronidase inhibitor tectorigenin isolated from the flower of Pueraria thunbergiana protects carbon tetrachloride-induced liver injuryLIVER INTERNATIONAL, Issue 4 2003Hae-Woong Lee Abstract Background/Aim: To understand the relationship between the fluctuation in serum ,-glucuronidase and hepatotoxicity, an inhibitor of ,-glucuronidase was isolated from the flowers of Pueraria thunbergiana and its hepatoprotective activity was measured. Method: Tectorigenin was isolated from the flowers of pueria thunbergiana as an inhibitor of ,-glucuronidase, and serum ALT, AST and biological parameters as markers for its hepatoprotective activity were measured on CCl4 -induced liver injury in mice. The relationship between serum ,-glucuronidase and hepatoprotective activities in mice was measured. Results: When tectorigenin at a dose of 100 mg/kg was intraperitoneally administered on CCl4 -induced liver injury in mice, it significantly inhibited the increase of plasma ALT, AST and LDH activities. The inhibitory effect of tectorigenin is much more potent than that of dimethyl diphenyl bicarboxylate (DDB), which has been used as a commercial hepatoprotective agent. When tectoridin transformed to tectorigenin by intestinal bacteria was orally administered to mice, it showed hepatoprotective activity. However, when tectoridin was intraperitoneally administrated to mice, it did not exhibit hepatoprotective activity. Moreover, orally administered tectoridin not only inhibited ,-glucuronidase but also increased GSH content and GST activity on CCl4 -induced hepatotoxicity of mice. Conclusion: We insist that an inhibitor of ,-glucuronidase tectorigenin may be hepatoprotective and tectoridin should be a prodrug transformed to tectorigenin. [source] |