Effects of extract from Ginkgo biloba on carbon tetrachloride-induced liver injury in rats

He, Shuixiang; Luo, Jin-Yan; Wang, Yuepeng; Wang, Yanli; Fu, Han; Xu, Junli; Zhao, Guoqiang; Liu, Enqi

doi:10.3748/wjg.v12.i24.3924

Cited by 45 publications

(28 citation statements)

References 33 publications

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“…It was found that chronic administration of CCl 4 induced a significant increase (2.4‐fold) in the liver content of TBARS 9 weeks after starting CCl 4 intoxication compared with the control group. Similar observations have been reported previously 40,44,45 …”

Section: Discussionsupporting

confidence: 93%

“…Similar observations have been reported previously. 40,44,45 Oral treatment of animals with lisinopril, fosinopril or losartan significantly counteracted GSH depletion and lipid peroxidation induced by CCl 4 . However, fosinopril treatment did not show any significant improvement in liver GSH levels compared with the CCl 4 -intoxicated group.…”

Section: Discussionmentioning

confidence: 98%

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Inhibition of the Renin–angiotensin System Attenuates the Development of Liver Fibrosis and Oxidative Stress in Rats

El‐Demerdash

Abdel-Salam²,

El-Batran³

et al. 2007

Clin Exp Pharma Physio

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1. The present study was designed to investigate the potential antifibrotic and anti-oxidant effects of lisinopril, fosinopril and losartan in an experimental rat model of liver injury using carbon tetrachloride (CCl(4)). 2. First, the potential hepatoprotective dose of each drug was screened against CCl(4)-induced acute hepatotoxicity. Then, we chose the minimum hepatoprotective dose of each drug to further investigate the mechanisms involved in the hepatoprotection using a chronic model of hepatotoxicity induced by CCl(4). 3. Liver function was assessed in addition to histopathological examination. Furthermore, oxidative stress markers (reduced glutathione (GSH) and lipid peroxides levels) and markers of fibrosis (hydroxyproline content and liver fibrosis area) were assessed. 4. It was found that treatment of animals with different drugs concomitantly with CCl(4) significantly counteracted the changes in liver function induced by CCl(4) (except fosinopril). In addition, the drugs ameliorated the histopathological changes induced by CCl(4). All drugs significantly counteracted lipid peroxidation and GSH depletion (except fosinopril) compared with the CCl(4)-intoxicated group. Moreover, the drugs studied significantly reduced liver hydroxyproline levels and the area of fibrosis compared with the CCl(4)-intoxicated group. 5. In conclusion, the present study provides evidence for the hepatoprotective effect of lisinopril, fosinopril and losartan. Both lisinopril and losartan was found to have better hepatoprotective potential than fosinopril against CCl(4)-induced hepatotoxicity. These hepatoprotective effects can be explained on the basis of anti-oxidant and antifibrotic mechanisms, mainly enhancement of GSH and reduction of lipid peroxidation and fibrosis.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 98%

Inhibition of the Renin–angiotensin System Attenuates the Development of Liver Fibrosis and Oxidative Stress in Rats

El‐Demerdash

Abdel-Salam²,

El-Batran³

et al. 2007

Clin Exp Pharma Physio

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“…CCl 4 is a potent hepatoxin producing centrilobular hepatic necrosis which is widely used for animal models of liver fibrosis. It has been reported that CYP450 in rat liver activates CCl 4 to a trichloromethyl free radical (CCl3• and/or CCl3OO•), and stimulates Kupffer cells to produce ROS, such as •O 2 − , H 2 O 2 and •OH, which damage the liver [9]–[11]. These ROS are eliminated by antioxidant enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and CAT.…”

Section: Introductionmentioning

confidence: 99%

The Protective Effect of Glycyrrhetinic Acid on Carbon Tetrachloride-Induced Chronic Liver Fibrosis in Mice via Upregulation of Nrf2

et al. 2013

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This study was designed to investigate the potentially protective effects of glycyrrhetinic acid (GA) and the role of transcription factor nuclear factor-erythroid 2(NF-E2)-related factor 2 (Nrf2) signaling in the regulation of Carbon Tetrachloride (CCl4)-induced chronic liver fibrosis in mice. The potentially protective effects of GA on CCl4-induced chronic liver fibrosis in mice were depicted histologically and biochemically. Firstly, histopathological changes including regenerative nodules, inflammatory cell infiltration and fibrosis were induced by CCl4.Then, CCl4 administration caused a marked increase in the levels of serum aminotransferases (GOT, GPT), serum monoamine oxidase (MAO) and lipid peroxidation (MDA) as well as MAO in the mice liver homogenates. Also, decreased nuclear Nrf2 expression, mRNA levels of its target genes such as superoxide dismutase 3 (SOD3), catalase (CAT), glutathione peroxidase 2 (GPX2), and activity of cellular antioxidant enzymes were found after CCl4 exposure. All of these phenotypes were markedly reversed by the treatment of the mice with GA. In addition, GA exhibited the antioxidant effects in vitro by on FeCl2-ascorbate induced lipid peroxidation in mouse liver homogenates, and on DPPH scavenging activity. Taken together, these results suggested that GA can protect the liver from oxidative stress in mice, presumably through activating the nuclear translocation of Nrf2, enhancing the expression of its target genes and increasing the activity of the antioxidant enzymes. Therefore, GA may be an effective hepatoprotective agent and viable candidate for treating liver fibrosis and other oxidative stress-related diseases.

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“…Carbon tetrachloride (CCl 4 ) is an effective hepatotoxic agent under laboratory experimentations causes oxidative damages in experimental animal models. CCl 4 react with membrane lipids and converting into trichloromethyl radical (.CCl 3 ) and finally liver cells fibrosis during chronic cases [1, 2]. Multiple reports revealed that these free radicles also depleted the antioxidant enzymatic and non-enzymatic levels which are linked to hepatic injuries and fibrosis [3].…”

Section: Introductionmentioning

confidence: 99%

Evaluation of Rumex hastatus leaves against hepatic fibrosis: a rat model

Sahreen

Khan

2017

BMC Complement Altern Med

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Background Rumex hastatus leaves have been widely used as food additive and for the treatment of various liver ailments. According to our previous studies, ethyle acetate (ERL) and methanolic (MRL) fractions of R. hastatus leaves are an accessible source of natural antioxidants. In the present research work we arranged to investigate the R. hastatus leaves as hepaptoprotective agent verse hepatic damages caused by CCl4.MethodsDuring this project we divided 48 rats into eight groups randomly. CCl4-induced damages were assessed through liver function markers viz.; alkaline phosphatase (ALP), alanine transaminase (ALT), aspartate transaminase (AST), γ-glutamyltransferase (γ-GT) and lactate dehydrogenase (LDH). Changes in lipid profile were checked by measuring serum total cholesterol (TC), triglycerides (Tg), high density lipoproteins (HDL) and low density lipoproteins (LDL). Antioxidant status was checked by the activities of antioxidant enzymes, DNA damages and cellular abnormalities at histo level.ResultsAdministration of CCl4 in rats caused significant increase in liver function and lipid profile indicating hepatic damages which were restored by co-administration of R. hastatus extracts. Cellular and DNA damages in hepatic tissues were caused by CCl4 which shown clear hepatic fibrosis in addition to disturb antioxidant enzyme level. Co-treatment with various fractions of R. hastatus leaves regulated these markers of oxidative dysfunctions.ConclusionFrom the present report it was inferred that R. hastatus leaves have the ability to reverse CCl4 - induced hepatic damages.

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Effects of extract from Ginkgo biloba on carbon tetrachloride-induced liver injury in rats

Abstract: EGb resists oxidative stress and thereby reduces chronic liver injury and liver fibrosis in rats with liver injury induced by CCl(4).

Cited by 45 publications

References 33 publications

Inhibition of the Renin–angiotensin System Attenuates the Development of Liver Fibrosis and Oxidative Stress in Rats

Inhibition of the Renin–angiotensin System Attenuates the Development of Liver Fibrosis and Oxidative Stress in Rats

The Protective Effect of Glycyrrhetinic Acid on Carbon Tetrachloride-Induced Chronic Liver Fibrosis in Mice via Upregulation of Nrf2

Evaluation of Rumex hastatus leaves against hepatic fibrosis: a rat model

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