Carbon tetrachloride-induced lipid peroxidation and hyperglycemia in rat

Khan, Rahmat Ali; Khan, Muhammad Rashid; Sahreen, Sumaira; Ahmed, Mushtaq; Shah, Naseer Ali

doi:10.1177/0748233713475503

Cited by 23 publications

(16 citation statements)

References 27 publications

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“… 39 In the same vein, intraperitoneal treatment with CCl 4 elicited hyperglycemia which was significantly (p < 0.05, p < 0.001 and p < 0.0001) reduced dose-dependently by oral treatments with 125–500 mg/kg/day of MIASE. Although, earlier studies have reported CCl 4 -induced hyperglycemia in rats treated with CCl 4 , 37,40,41 the marked reduction in FBG values, suggests the antihyperglycemic potential of MIASE in CCl 4 -induced hyperglycemia in rats. Although several studies have independently reported the antihyperglycemic effect of MIASE in different diabetic rat models , 3,4,42 this study reports for the first time the hypoglycemic effect of MIASE in the CCl 4 -induced hepatotoxic rats.…”

Section: Discussionmentioning

confidence: 77%

Modulatory potentials of the aqueous stem bark extract of Mangifera indica on carbon tetrachloride-induced hepatotoxicity in rats

Adeneye

Awodele

Aiyeola

et al. 2015

Journal of Traditional and Complementary Medicine

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Among Yoruba herbalists (Southwest Nigeria), hot water infusion of Mangifera indica L. (芒果 Máng Guǒ) stem bark is reputedly used for the treatment of fever, jaundice and liver disorders. The present study, therefore, investigates the protective effects and mechanism(s) of chemopreventive and curative effects of 125–500 mg/kg/day of Mangifera indica aqueous stem bark extract (MIASE) in acute CCl4-induced liver damage in rats. Rats were treated intragastrically with 125, 250 and 500 mg/kg/day of MIASE for 7 days before and after the administration of CCl4 (3 ml/kg of 20% CCl4, i.p.). The serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total protein (TP), albumin (ALB), triglyceride (TG), total cholesterol (TC), high density lipoprotein cholesterol (HDL-c), low density lipoprotein cholesterol (LDL-c), total bilirubin (TB), conjugated bilirubin (CB) and fasting blood glucose (FBG) levels were estimated. In addition, hepatic tissue reduced glutathione (GSH) and the malondialdehyde (MDA) concentrations, catalase (CAT), superoxide (SOD) activities in the hepatic homogenate, and histopathological changes in the rat liver sections were determined. Preliminary qualitative phytochemical screening for bioactive compounds in MIASE was also conducted. Results showed that oral treatment with 125–500 mg/kg/day of MIASE significantly attenuated the increase in serum ALT, AST, ALP, FBG, TB, CB and LDL-c levels in acute liver injury induced by CCl4 treatment. Findings also revealed significant elevations in the serum TC, TG, HDL-c, TP and ALB levels. There was marked architectural remodeling in the hepatic lesions of hepatocyte vacuolation and centrilobular necrosis induced by CCl4 treatment, coupled with significant weight loss. MIASE also markedly enhanced SOD and CAT activities while reducing MAD formation; and increased GSH concentration in the hepatic homogenate compared with untreated CCl4-intoxicated group, with more protection offered in the curative than the chemopreventive models of CCl4 hepatotoxicity. Thus, these results indicate that MIASE has a profound protective effect against acute CCl4-induced hepatotoxicity in rats, which may be due to its free radicals scavenging effect, inhibition of lipid peroxidation, and its ability to increase antioxidant activity.

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Section: Discussionmentioning

confidence: 77%

Modulatory potentials of the aqueous stem bark extract of Mangifera indica on carbon tetrachloride-induced hepatotoxicity in rats

Adeneye

Awodele

Aiyeola

et al. 2015

Journal of Traditional and Complementary Medicine

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“…The chemicals commonly used to cause hepatic lesions and induce liver fibrosis include ethanol, carbon tetrachloride (CCl 4 )[52], thioacetamide[53], dimethylnitrosamine[54], and diethylnitrosamine[55]. A number of specific diets, such as the methionine- and choline-deficient diet[56], high-fat diet[57], and choline-deficient L -amino acid-defined diet[58], can be used to induce progression of NAFLD to hepatic fibrosis in experimental animals.…”

Section: Etiology and Pathological Characteristics Of Hepatic Fibrosismentioning

confidence: 99%

Liver fibrosis and hepatic stellate cells: Etiology, pathological hallmarks and therapeutic targets

Zhang¹,

Yuan²,

He³

et al. 2016

WJG

466

327

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Liver fibrosis is a reversible wound-healing process aimed at maintaining organ integrity, and presents as the critical pre-stage of liver cirrhosis, which will eventually progress to hepatocellular carcinoma in the absence of liver transplantation. Fibrosis generally results from chronic hepatic injury caused by various factors, mainly viral infection, schistosomiasis, and alcoholism; however, the exact pathological mechanisms are still unknown. Although numerous drugs have been shown to have antifibrotic activity in vitro and in animal models, none of these drugs have been shown to be efficacious in the clinic. Importantly, hepatic stellate cells (HSCs) play a key role in the initiation, progression, and regression of liver fibrosis by secreting fibrogenic factors that encourage portal fibrocytes, fibroblasts, and bone marrow-derived myofibroblasts to produce collagen and thereby propagate fibrosis. These cells are subject to intricate cross-talk with adjacent cells, resulting in scarring and subsequent liver damage. Thus, an understanding of the molecular mechanisms of liver fibrosis and their relationships with HSCs is essential for the discovery of new therapeutic targets. This comprehensive review outlines the role of HSCs in liver fibrosis and details novel strategies to suppress HSC activity, thereby providing new insights into potential treatments for liver fibrosis.

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“…RSME prevented renal injuries with a subsequent restoration of all these parameters discussed above. This study is in relation to the studies of Khan, Khan [26] and Venkatanarayana, Sudhakara [27] who investigated how the administration of CCl 4 caused marked oxidative stress in kidneys. Serum creatinine, total bilirubin, gamma-GT and urea concentrations were significantly higher in the CCl 4 -treated rats.…”

Section: Discussionmentioning

confidence: 88%

In vivo Antioxidant Potential of Raphanus sativus Seeds in Rat Kidney Against CCl4-Induced Toxicity

Shehzadi¹,

Shah²,

Khan³

et al. 2019

Pol. J. Environ. Stud.

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In this study, the methanolic extract of Raphanus sativus (RSME) seeds was evaluated for its protective effect against CCl 4-induced nephrotoxicity. The treatment of Swiss albino rats with intraperitoneal injections of CCl 4 (1 ml/kg body weight) on alternate days for 30 days decreased the antioxidant enzymes, while lipid peroxidation and serum toxicity markers were increased. These changes were reversed in the animals receiving an oral dose of RSME (100 and 200 mg/kg body weight) along with CCl 4 , thus increasing the level of antioxidant enzymes and decreasing serum toxicity markers and thus ameliorating the toxic effect of CCl 4. These results show that seed extract of R. sativus can reciprocate the toxic effects of CCl 4 and can be used to make a chemopreventive drug.

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Carbon tetrachloride-induced lipid peroxidation and hyperglycemia in rat

Cited by 23 publications

References 27 publications

Modulatory potentials of the aqueous stem bark extract of Mangifera indica on carbon tetrachloride-induced hepatotoxicity in rats

Modulatory potentials of the aqueous stem bark extract of Mangifera indica on carbon tetrachloride-induced hepatotoxicity in rats

Liver fibrosis and hepatic stellate cells: Etiology, pathological hallmarks and therapeutic targets

In vivo Antioxidant Potential of Raphanus sativus Seeds in Rat Kidney Against CCl4-Induced Toxicity

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