Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.1.109 (AST)
 6,066 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ethanol has been known to cause injury to the liver and other tissues; however the molecular factors responsible for alcohol induced liver injury has not been fully understood. Recent studies indicate that reactive oxygen species (ROS) may play an important role in alcohol induced liver injury. Peroxisome proliferator activated receptor-gamma (PPAR-gamma)-coactivator 1alpha (PGC-1alpha) has been shown to be involved in defenses against ROS by inducing many ROS-detoxifying enzymes. However, the role of PGC-1alpha in alcohol induced liver injury has not been elucidated. Therefore, in this study, we examined the effect of alcohol on gene and protein expression of PGC-1alpha in H4-IIE cells (in vitro) and hepatic tissues (in vivo) by real-time PCR and Western blot, respectively. Our results show that exposure to 500 mM ethanol in H4-IIE cells for 24 h significantly decreased both gene and protein expression of PGC-1alpha. PGC-1alpha gene expression was significantly decreased in cells exposed to 100 ng/ml LPS or 1% hypoxia for 24 h. In addition, PGC-1alpha gene and protein expressions were slightly lower in hepatic tissues of rats exposed to ethanol for 15 h, at the level equivalent to the 500 mM used in culture cells, in comparison to sham rats. In contrast, serum LDH and AST levels in ethanol exposed rats were 1.9 fold and 2.8 fold higher than that of sham rats, respectively, which suggest significant organ injury in these rats following ethanol exposure. Likewise, catalase, an enzyme that hydrolyzes peroxide to water, is significantly increased in ethanol exposed H4-IIE cells which further confirms ROS generation due to ethanol exposure. Thus, our results show that oxidative stress conditions such as acute alcohol consumption, LPS or hypoxia suppresses PGC-1alpha expression in the liver, thereby presumably downregulates pertinent ROS-scavenging enzymes and enhances liver injury.
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PMID:Suppression of PGC-1alpha by Ethanol: Implications of Its Role in Alcohol Induced Liver Injury. 1907 70

The present study was undertaken to evaluate the cardioprotective potential of tetrahydrocurcumin (THC) and rutin in an in vivo rat ischemia-reperfusion (I/R) model of myocardial infarction (MI). Male wistar rats were divided into six groups receiving saline (control MI/R group), vehicle control MI/R group, THC (5 mg kg(-1) and 10 mg kg(-1)) and rutin (5 mg kg(-1) and 10 mg kg(-1)) i.p. injection respectively. At the day of the experiment, each group was subjected to acute ischemia for 30 min by occlusion of the left anterior descending coronary artery (LAD). Thereafter reperfusion was allowed for 4 h. MI/R resulted in significant cardiac necrosis, elevation in lipid peroxidation, elevation in cardiac marker enzymes AST, ALT and decline in antioxidant status catalase, reduced glutathione in the normal control MI/R group and vehicle control MI/R group. Myocardial infarction produced after MI/R was significantly reduced in tetrahydrocurcumin and rutin of the myocardial antioxidant status, infarct size reduction compared to control and vehicle control MI/R group. Furthermore, MI/R induced lipid peroxidation was significantly reduced by tetrahydrocurcumin and rutin. Cardioprotection in the treatment group was probably a result from suppression of oxidative stress. Histopathological examination further confirmed the protective effect of tetrahydrocurcumin and rutin on the MI/R heart.
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PMID:Cardioprotective effect of tetrahydrocurcumin and rutin on lipid peroxides and antioxidants in experimentally induced myocardial infarction in rats. 1932 Feb 87

Alcohol consumption is implicated in the genesis of a spectrum of liver abnormalities, which are associated with a number of factors. In the present study, time-dependent effects of ethanol on cytokines (TNF-alpha, IL-2, IL-4, IL-10, IFN-gamma, VEGF-A and TGF-beta1) in serum, and blood oxidative stress parameters such as reduced glutathione content, TBARS level and activities of GPx, GR, GST, catalase and SOD in 8-10 weeks-old male BALB/c mice have been investigated. Ethanol administered @ 1.6 g/kg body wt/day significantly increased the activities of liver marker enzymes AST, ALT and ALP. Serum nitrite levels and haemolysate TBARS level also increased, while total antioxidant status in serum and GSH content in whole blood hemolysate decreased from 4th week onwards of exposure. In spite of the increased serum nitrite level and GST activity in the haemolysate, albumin level in serum, GPx and GR activities in haemolysate decreased after 12 weeks of exposure. Chronic ethanol treatment did not show any effect on IL-2, but IL-4 level was reduced and other cytokines such as IL-10, TNF-alpha, IFN-gamma, TGF-beta1 and VEGF-A levels were increased significantly after 12 weeks. The study indicates a relationship between free radical generation and immune response, and suggests that ethanol-induced liver damage is associated with oxidative stress and immunological alterations in a time-dependent manner.
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PMID:Time-dependent effects of ethanol on blood oxidative stress parameters and cytokines. 1937 64

This study aimed to evaluate the effect of phenolic extract and purified hydroxytyrosol (HT) from olive mill waste (OMW) on oxidative stress and hyperglycemia in alloxan-induced diabetic rats. The OMW biophenols were extracted using ethyl acetate. The obtained extract was fractionated by solid phase extraction (SPE) experimentation to generate two fractions: (F1) and (F2). HPLC-UV and HPLC-MS analysis showed that (F1) was made of known OMW monomeric phenolics mainly hydroxytyrosol (HT) while (F2) contained oligomeric and polymeric phenols such as verbascosid and ligstrosid. (HT) was purified from (F1) using silica gel-column chromatography and silica gel-TLC techniques. In incubated pancreas, supplementation of OMW fractions enhanced insulin secretion. The administration of OMW extract fractions (F1) and (F2) as well as purified (HT) in diabetic rats caused a decrease in glucose level in plasma and an increase in renal superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) activities in liver and kidney. Furthermore, a protective action against hepatic and renal toxicity in diabetic rats was clearly observed. Furthermore, a significant decrease in hepatic and renal indices toxicity was observed, i.e. alkalines phosphatases (ALP), aspartate and lactate transaminases (AST and ALT) activities and the thiobarbituric acid-reactive substances (TBARs), total and direct bilirubin, creatinine and urea levels. In addition, (F1), (F2) and especially (HT) decreased triglycerides (TG), total-cholesterol (T-Ch) and higher HDL-cholesterol (HDL-Ch) in serum. These beneficial effects of OMW biophenols were confirmed by histological findings in hepatic, renal and pancreatic tissues of diabetic rats. This study demonstrates for the first time that OMW polyphenols and especially (HT) are efficient in inhibiting hyperglycemia and oxidative stress induced by diabetes and suggests that administration of HT may be helpful in the prevention of diabetic complications associated with oxidative stress.
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PMID:Hypoglycemic and antioxidant effects of phenolic extracts and purified hydroxytyrosol from olive mill waste in vitro and in rats. 1939 37

The study investigated the protective effect of electrolyzed reduced water (ERW) against carbon tetrachloride (CCl(4))-induced liver damage. Male ICR mice were randomly divided into control, CCl(4), CCl(4)+silymarin, and CCl(4)+ERW groups. CCl(4)-induced liver lesions include leukocytes infiltration, hepatocyte necrosis, ballooning degeneration, mitosis, calcification, fibrosis and an increase of serum alanine aminotransferase (ALT), and aminotransferase (AST) activity. In addition, CCl(4) also significantly decreased the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). By contrast, ERW or silymarin supplement significantly ameliorated the CCl(4)-induced liver lesions, lowered the serum levels of hepatic enzyme markers (ALT and AST) and increased the activities of SOD, catalase, and GSH-Px in liver. Therefore, the results of this study show that ERW can be proposed to protect the liver against CCl(4)-induced oxidative damage in mice, and the hepatoprotective effect might be correlated with its antioxidant and free radical scavenging effect.
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PMID:Hepatoprotective effect of electrolyzed reduced water against carbon tetrachloride-induced liver damage in mice. 1947 16

In the current study, the effect of Ajuga iva extract on blood glucose, lipid profile, hepatic and renal toxicity and antioxidant enzyme activities in alloxan-induced diabetic rats was investigated. Diabetes was confirmed by measuring the glucoserua concentration 15 days after alloxan administration. Ajuga iva extract was administrated orally 3 weeks after alloxan injection. Our results investigate that Ajuga iva extract supplementation increased the levels of both enzymatic antioxidant (superoxide dismutase, catalase and glutathione peroxidase) and metals antioxidants (iron, copper, magnesium, calcium) and decreased lipid peroxidation level (TBARs). Besides Ajuga iva ameliorated diabetes provoked hepatic and renal toxicity appeared by a lower level in total and direct bilirubin, urea, creatinine, triglyceride (TG), cholesterol and a higher level in HDL-cholesterol. Besides, the activities of phosphatase alkalines (PAL), aspartate and lactate transaminase (AST & ALT) were decreased. The benefices effects of phytoecdysteroids of Ajuga iva confirmed by histological observation in pancreatic tissues. In conclusion, Ajuga iva phytoecdysteroids supplements seem to be beneficial for correcting the hyperglycemia and preventing diabetic complications in liver, pancreas and kidneys.
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PMID:Therapeutic effect of phytoecdysteroids rich extract from Ajuga iva on alloxan induced diabetic rats liver, kidney and pancreas. 1947 20

Fluorosis is a serious public health problem in many parts of the world. As in the case of many chronic degenerative diseases, increased production of reactive oxygen species has been considered to play an important role, even in the pathogenesis of chronic fluoride toxicity. Black berry is closely linked to its protective properties against free radical attack. Therefore, the aim of this study was to demonstrate the role of black berry juice (BBJ) in decreasing the hepatotoxicity and oxidative stress of sodium fluoride (NaF). Results showed that NaF caused elevation in liver TBARS and nitric oxide (NO), and reduction in superoxide dismutase (SOD), catalase (CAT), total antioxidant capacity (TAC) and glutathione (GSH). Plasma transaminases (AST and ALT), creatine kinase (CK), lactate dehydrogenase (LDH), total lipids (TL), cholesterol, triglycerides (TG), and low density lipoprotein-cholesterol (LDL-c) were increased, while high density lipoprotein-cholesterol (HDL-c) was decreased. On the other hand, BBJ reduced NaF-induced TBARS, NO, TL, cholesterol, TG, LDL-c, AST, ALT, CK and LD. Moreover, it ameliorated NaF-induced decrease in SOD, CAT, GSH, TAC and HDL-c. Therefore, the present results revealed that BBJ has a protective effect against NaF-induced hepatotoxicity by antagonizing the free radicals generation and enhancement of the antioxidant defence mechanisms.
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PMID:Mitigating effects of antioxidant properties of black berry juice on sodium fluoride induced hepatotoxicity and oxidative stress in rats. 1954 Aug 98

The possible modulatory effect of methanolic extract of Vernonia amygdalina (MEVA), a plant widely consumed in the tropics and used locally in the treatment of fever, jaundice, stomach disorders and diabetes on the toxicity of CCl(4), was investigated in male rats. Oral administration of CCl(4) at a dose of 1.2g/kg body weight 3 times a week for 3 weeks significantly induced marked hepatic injury as revealed by increased activity of the serum enzymes ALT, AST, SALP and gamma-GT. Methanolic extract of V. amygdalina administered 5 times a week for 2 weeks before CCl(4) treatment at 250 and 500 mg/kg doses of the extract ameliorated the increase in the activities of these enzymes. Likewise the methanolic extract of V. amygdalina reduced the CCl(4)-induced increase in the concentrations of cholesterol, triglyceride and phospholipid by 37.8%, 30.6% and 8.5%, respectively, and a reduction in the cholesterol/phospholipids ratio. These parameters were however increased at 750 mg/kg extract pretreatment. CCl(4)-induced lipid peroxidation was likewise attenuated by 57.2% at 500 mg/kg dose of the methanolic extract of V. amygdalina. Similarly, administration of the extract increased the activities of the antioxidant enzymes: superoxide dismutase, glutathione S-transferase and reduced glutathione concentration significantly at 500 mg/kg (P<0.05) and catalase activity at 500-1000 mg/kg doses. These results suggest that methanolic extract of V. amygdalina leaves posseses protective effect against CCl(4)-induced hepatotoxicity by the antioxidant mechanism of action.
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PMID:Hepatoprotective effects of Vernonia amygdalina (astereaceae) in rats treated with carbon tetrachloride. 1958 Oct 77

Cinnamon is used to flavor most foods in Arabian countries. The aim of this study was to evaluate the medicinal importance, reflecting an important trend in research. The hepatoprotective activity of aqueous and ethanolic extracts of cinnamon was investigated against carbon tetrachloride (CC1(4)) induced lipid peroxidation and hepatic injury in rats. The elevated serum AST and ALT enzymatic activities induced by CC1(4) were significantly restored to near normal by oral administration of 200 mg/kg of either extracts once daily for 7 days, as compared to untreated rats. There was a significant elevation in the level of liver malondialdhyde (MDA), while the activities of antioxidant enzymes superoxide dismutase and catalase (SOD and CAT) were significantly decreased in CC1(4) intoxicated rats. The results obtained indicated that ethanolic extract has more potent hepatoprotective action than water extract against CC1(4) by lowering the MDA level and elevating antioxidants enzymes activities (SOD and CAT). The possible mechanism of this activity may be free radical-scavenging polyphenol compounds. The hepatoprotective properties were documented by the histopathological data obtained. Consequently, this extract can be used as a therapeutic regime in treatment of some hepatic disorders without any side effects. Further study will be done for separation and identification of active components and for testing antitumor activity.
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PMID:Hepatoprotective effect of cinnamon extracts against carbon tetrachloride induced oxidative stress and liver injury in rats. 1962 Nov 36

The role of oxidative stress in the pathogenesis of alcoholic diseases in the liver is well documented. Kolaviron (KV), a biflavonoid complex from Garcinia kola seeds, possesses a variety of biological activities, including antioxidant. Our aim was to investigate in vivo whether KV may attenuate oxidative stress in liver of Wistar albino rats following chronic ethanol administration. Thirty-six male Wistar albino rats were randomly divided into six groups. Toxicity was induced by administering 7.5% or 45% ethanol at 3 g/kg of body weight daily for 8 weeks. Rats were treated with KV at 200 mg/kg of body weight for the same duration. Treatment was by oral gavage. Integrity of liver was assessed by determining the levels of serum alanine and aspartate aminotransferases (ALT and AST, respectively) and alkaline phosphatase (ALP). The antioxidant status was monitored by determining the levels of hepatic superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), reduced glutathione (GSH), and malondialdehyde (MDA), the end product of lipid peroxidation (LPO). Experimentally, chronic ethanol administration led to hepatotoxicity as evidenced by the increase in levels of serum ALT, AST, and ALP. Ethanol also enhanced the formation of MDA in the liver. Specifically, MDA was elevated by 70% and 98% in animals treated with 7.5% and 45% ethanol, respectively. Levels of hepatic SOD, CAT, GST, and GSH were significantly (P < .05) reduced by ethanol treatment. Co-administration of KV during ethanol treatment inhibited hepatic LPO and ameliorated SOD and GST activities. These findings demonstrated that KV could have a beneficial effect by inhibiting the oxidative damage in liver of Wistar rats caused by chronic ethanol administration.
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PMID:Effect of kolaviron, a biflavonoid complex from Garcinia kola seeds, on ethanol-induced oxidative stress in liver of adult wistar rats. 1962 7


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