Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ayurvedic and other 'traditional' medical practitioners in Sri Lanka use the mature leaves of the plant Osbeckia octandra for its hepatoprotective properties. In this study the effects of an aqueous extract of Osbeckia octandra against injury induced by D-galactosamine and tert-butyl hydroperoxide (TBH) were investigated in freshly isolated rat hepatocytes. The plant extract (500 micrograms/ml) significantly reduced the inhibition of protein synthesis (as assessed by the incorporation of 14C-leucine into protein) in hepatocytes incubated for 1 h with 10 mM galactosamine by a mean of 25.6 +/- 3.6% and decreased the release of cellular lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) enzyme activities into the medium by 55.3% and 32.8%, respectively. With TBH, the plant extract decreased lipid peroxidation (estimated from malondialdehyde formation) by a mean of 29.9 +/- 1.1% together with a 46.8% and 54.7% decrease in the release of LDH and AST, respectively into the incubation medium. Significant protection was also obtained when the Osbeckia extract was added to the incubation medium up to 30 min after pre-exposure of the hepatocytes to either galactosamine or, to a lesser extent, TBH. The results support the use of Osbeckia as a hepatoprotective agent.
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PMID:Protective effects of Osbeckia octandra against galactosamine and tert-butyl hydroperoxide induced hepatocyte damage. 884 86

Hibiscus anthocyanins (HAs), a group of natural pigments occurring in the dried flowers of Hibiscus sabdariffa L., which is a local soft drink material and medical herb, were studied for antioxidant bioactivity. The preliminary study showed that HAs were able to quench the free radicals of 1,1-diphenyl-2-picrylhydrazyl. This antioxidant bioactivitiy was further evaluated using the model of tert-butyl hydroperoxide (t-BHP)-induced cytotoxicity in rat primary hepatocytes and hepatotoxicity in rats. The results demonstrated that HAs, at the concentrations of 0.10 and 0.20 mg/ml, significantly decreased the leakage of lactate dehydrogenase and the formation of malondialdehyde induced by a 30-min treatment of t-BHP (1.5 mM). The in vivo investigation showed that the oral pretreatment of HAs (100 and 200 mg/kg) for 5 days before a single dose of t-BHP (0.2 mmol/kg, ip) significantly lowered the serum levels of hepatic enzyme markers (alanine and aspartate aminotransferase) and reduced oxidative liver damage. The histopathological evaluation of the liver revealed that Hibiscus pigments reduced the incidence of liver lesions including inflammatory, leucocyte infiltration, and necrosis induced by t-BHP in rats. Based on the results described above, we speculate that Hibiscus pigments may play a role in the prevention of oxidative damage in living systems.
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PMID:Protective effect of Hibiscus anthocyanins against tert-butyl hydroperoxide-induced hepatic toxicity in rats. 1076 26

Berberine, a main protoberberine component of Coptidis Rhizoma, was studied for the mechanism of its inhibitory effects on the tert-butyl hydroperoxide (t-BHP)-induced cytotoxicity and lipid peroxidation in rat liver. In the preliminary study, berberine expressed an antioxidant property by its capacity for quenching the free radicals of 1,1-diphenyl-2-picrylhydrazyl (DPPH). Further investigations were conducted using t-BHP-induced cytotoxicity in rat primary hepatocytes and hepatotoxicity in rats to evaluate the antioxidative bioactivity of berberine. The results in rat primary hepatocytes demonstrated that berberine, at the concentrations of 0.01-1.0 mM, significantly decreased the leakage of lactate dehydrogenase (LDH) and alanine aminotransferase (ALT), and the formation of malondialdehyde (MDA) induced by 30 min treatment of t-BHP (1.5 mM). Berberine also attenuated the t-BHP-induced depletion of glutathione (GSH) and induced a high level of DNA repair synthesis. The in vivo study showed that the intraperitoneal pretreatment with berberine (0.5 and 5 mg/kg) for 5 days before a single dose of t-BHP (0.1 mmol/kg) significantly lowered the serum levels of hepatic enzyme markers (ALT and aspartate aminotransferase) and reduced oxidative stress in the liver. The histopathological evaluation of the livers revealed that berberine reduced the incidence of liver lesions, including hepatocyte swelling, leukocyte infiltrations, and necrosis induced by t-BHP. These results lead us to speculate that berberine may play a chemopreventive role via reducing oxidative stress in living systems.
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PMID:Inhibitory effect of berberine on tert-butyl hydroperoxide-induced oxidative damage in rat liver. 1241 30

The aim of this study was to investigate the protective effect of acanthoic acid, a diterpene isolated from the root bark of Acanthopanax koreanum, on liver injury induced by either tert-butyl hydroperoxide (tBH) or carbon tetrachloride in vitro and in vivo. In vitro, the cellular leakage of lactate dehydrogenase (LDH) following treatment with 1.5 mM tBH for 1 h, was significantly inhibited by co-treatment with acanthoic acid (25 and 5 microg/mL) and the ED (50) of acanthoic acid was 2.58 microg/mL (8.5 microM). The cellular leakage of LDH following one hour of treatment with 2.5 mM CCl (4) was significantly inhibited by co-treatment with acanthoic acid (25 microg/mL) and the ED (50) of acanthoic acid was 4.25 microg/mL (14.1 microM). Co-treatment with acanthoic acid significantly inhibited the generation of intracellular reactive oxygen species (ROS) and intracellular glutathione (GSH) depletion induced by tBH or CCl (4). Acanthoic acid pretreatment (100 mg/kg per day for four consecutive days, p. o.) significantly reduced levels of aspartate transaminase and alanine transaminase in acute liver injury models induced by either tBH or carbon tetrachloride. Treatment with acanthoic acid (100 mg/kg, p. o.) at 6, 24, and 48 hours after carbon tetrachloride subcutaneous injection significantly reduced the levels of aspartate transaminase and alanine transaminase in serum. Histological observations revealed that fatty acid changes, hepatocyte necrosis and inflammatory cell infiltration in CCl (4)-injured liver were improved upon treatment with acanthoic acid. In vivo treatment with acanthoic acid was not able to modify CYP2E1 activity and protein expression in liver microsomes at the dose used, showing that the hepatoprotective effect of acanthoic acid was not mediated through inhibition of CCl (4) bioactivation. From the results above, acanthoic acid had a protective effect against tBH- or CCl (4)-induced hepatotoxicity in vitro and in vivo.
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PMID:Acanthoic acid from Acanthopanax koreanum protects against liver injury induced by tert-butyl hydroperoxide or carbon tetrachloride in vitro and in vivo. 1509 47

There is increasing evidence that oxidative stress is implicated in the pathogenesis of various diseases, including alcoholic liver injury. In the present work, we investigate the protective effects of the saponins isolated from the roots of Platycodon grandiflorum A. DC (Campanulaceae), Changkil saponins (CKS), on the tert-butyl hydroperoxide (t-BHP)-induced oxidative injury (hepatotoxicity) in cultured rat primary hepatocytes and in rat livers. CKS significantly reduced t-BHP-induced oxidative injuries in cultured rat hepatocytes, as determined by cell cytotoxicity, intracellular glutathione (GSH) content and lipid peroxidation in a dose-dependent manner. CKS provided good protection from the t-BHP-induced production of intracellular reactive oxygen species and DNA damage. In addition, CKS was able to quench 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radicals and the superoxide radical. The in vivo study showed that the pretreatment with CKS prior to the administration of t-BHP significantly prevented the increase in the serum levels of hepatic enzyme markers (alanine aminotransferase and aspartate aminotransferase) and reduced oxidative stress, such as GSH content and lipid peroxidation, in the liver in a dose-dependent manner. These results support the anti-oxidative role of CKS, and demonstrate that CKS can scavenge oxygen free radicals and protect cells from oxidative stress.
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PMID:Protective effect of saponins derived from roots of Platycodon grandiflorum on tert-butyl hydroperoxide-induced oxidative hepatotoxicity. 1510 19

The protective effect of Hsian-tsao (Mesona procumbens Hemsl.) and its active compounds on liver damage was evaluated using the model of tert-butyl hydroperoxide (t-BHP)-induced acute hepatic damage in rats. Male Sprague-Dawley rats (200 +/- 10 g) were orally pretreated with a water extract of Hsian-tsao (WEHT) (0.1, 0.5, and 1.0 g/kg) or caffeic acid (0.1 g/kg of body weight) for 13 days before a single dose of t-BHP (0.2 mmol/kg, intraperitoneally) to each animal, and the rats were sacrificed 18 h later by decapitation; blood samples were collected for the assays of serum biochemical values. The livers were excised from the animals and assayed for oxidative injury, antioxidant enzyme, and pathological histology. The result showed that the oral pretreatment of WEHT (0.1, 0.5, and 1.0 g/kg) or caffeic acid (0.10 g/kg) before t-BHP (0.2 mmol/kg) treatment significantly lowered the serum levels of the hepatic enzyme markers (alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase) and reduced oxidative stress of the liver by evaluation of malondialdehyde, glutathione, 8-hydroxy-2'-deoxyguanosine, glutathione peroxidase, and glutathione reductase. The histopathological evaluation of the rat livers showed that WEHT and caffeic acid reduced the incidence of liver lesions including cloudy swelling, pyknosis, and cytolysis induced by t-BHP in rats. On the basis of the results of this study, it can be speculated that M. procumbens protects liver against t-BHP-induced hepatic damage in rats.
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PMID:Protective effect of Mesona procumbens against tert-butyl hydroperoxide-induced acute hepatic damage in rats. 1521 57

To clarify the hepatoprotective effects of kakkalide and its metabolite irisolidone by human fecal microflora, their effects on tert-butyl hydroperoxide (t-BHP)-injured HepG2 cells and mice were investigated. Irisolidone protected HepG2 cells against cytotoxicity induced by t-BHP. However, kakkalide did not protect cytotoxicity. When kakkalide 100 mg/kg was orally administered to mice injured by t-BHP, it significantly inhibited the increase in plasma alanine aminotransferase and aspartate aminotransferase activities by 84% and 85% of t-BHP-treated control group, respectively. The inhibitory effect of kakkalide is much more potent than that of silybin, a hepatoprotective agent. However, intraperitoneally administered kakkalide did not exhibit hepatoprotective activity. When irisolidone was intraperitoneally administered to mice, it exhibited potent hepatoprotective activity. Based on these findings, irisolidone can be hepatoprotective and kakkalide may be a prodrug transformed to irisolidone.
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PMID:Hepatoprotective effects of irisolidone on tert-butyl hyperoxide-induced liver injury. 1574 84

The aim of this study was to investigate the protective effect of (S)-bakuchiol isolated from the seed of Psoralea corylifolia, on liver injury. Primary rat hepatocyte intoxication was induced by tert-butyl hydroperoxide (tBH), carbon tetrachloride (CCl4) or D-galactosamine (D-GalN). Liver injury was induced by either CCl4 or D-GalN in rats. In vitro, the cellular leakage of lactate dehydrogenase and cell viability following treatment with hepatotoxicants were significantly improved by bakuchiol treatment at a concentration range of 25-200 microM for tBH, 100-200 microM for CCl4 and 100-200 microM for D-GalN-induced hepatocyte injury. Treatment with bakuchiol significantly inhibited lipid peroxidation and intracellular glutathione depletion in hepatocytes induced by tBH, CCl4 or D-GalN. Treatment with bakuchiol (25 or 50 mg/kg, p.o.) at 1, 24 and 48 h after subcutaneous injection of CCl4 significantly reduced the levels of aspartate transaminase and alanine transaminase in serum. Histological observations revealed that fatty acid changes, hepatocyte necrosis and inflammatory cell infiltration in CCl4-injured liver was improved when treated with bakuchiol. Bakuchiol treatment (25 and 50 mg/kg, p.o.) also significantly reduced the levels of aspartate transaminase and alanine transaminase in an acute liver injury model induced by D-GalN. From these results, bakuchiol has a protective effect against tBH, CCl4 or D-GalN-induced hepatotoxicity in vitro or in vivo.
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PMID:Protective effect of (S)-bakuchiol from Psoralea corylifolia on rat liver injury in vitro and in vivo. 1597 Nov 20

The ripe fruit of Terminalia chebula RETZIUS (T. chebula RETZ) (Combretsceae), which is a native plant in India and Southeast Asia, has traditionally been used as a popular folk medicine for homeostatic, antitussive, laxative, diuretic, and cardiotonic treatments. The objective of this study was to evaluate the protective effects of an aqueous extract of fruit of T. chebula on the tert-butyl hydroperoxide (t-BHP)-induced oxidative injury observed in cultured rat primary hepatocytes and rat liver. Both treatment and pretreatment of the hepatocytes with the T. chebula extract (TCE) significantly reversed the t-BHP-induced cell cytotoxicity and lactate dehydrogenase leakage. In addition, TCE exhibited in vitro ferric-reducing antioxidant activity and 2,2-diphenyl-1-picryhydrazyl free radical-scavenging activities. The in vivo study showed that pretreatment with TCE (500 or 1000 mg/kg) by gavage for 5 d before a single dose of t-BHP (0.1 mmol/kg i.p.) significantly lowered the serum levels of the hepatic enzyme markers aspartate aminotransferase and alanine aminotransferase and reduced the indicators of oxidative stress in the liver, such as the glutathine disulfide content and lipid peroxidation, in a dose-dependent manner. Histopathologic examination of the rat livers showed that TCE reduced the incidence of liver lesions, including hepatocyte swelling and neutrophilic infiltration, and repaired necrosis induced by t-BHP. Based on the results described above, we speculate that TCE has the potential to play a role in the hepatic prevention of oxidative damage in living systems.
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PMID:Antioxidant effects of aqueous extract of Terminalia chebula in vivo and in vitro. 1614 31

To evaluate the hepatoprotective effect of Red Ginseng (RG), we isolated a main constituent 20(S)-ginsenoside Rg3 from RG, and its metabolite 20(S)-ginsenoside Rh2 by human intestinal microflora, and investigated their hepatoprotective activities in tert-butyl hydroperoxide (t-BHP)-induced hepatotoxicity of HepG2 cells and mice. When HepG2 cells were treated with t-BHP, its cytotoxicity was significantly increased. 20(S)-Ginsenoside Rh2 potently protected its cytotoxicity, but 20(S)-ginsenoside Rg3 weakly protected it. Intraperitoneally and orally administered 20(S)-ginsenoside Rh2 to t-BHP-injured mice significantly inhibited the increase of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities. Orally administered 20(S)-ginsenoside Rg3 also showed the inhibition against the increase of ALT and AST of t-BHP-induced mice. However, intraperitoneally administered 20(S)-ginsenoside Rg3 could not inhibit the elevation of serum ALT and AST activities. These results suggest that 20(S)-ginsenoside Rg3 a main component of RG may be a prodrug for hepatotoxicity.
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PMID:Hepatoprotective effect of 20(S)-ginsenosides Rg3 and its metabolite 20(S)-ginsenoside Rh2 on tert-butyl hydroperoxide-induced liver injury. 1620 63


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