Effect of Acer tegmentosum Maxim. Extracts on Acute Hepatitis and Fatty Liver in Rats

Seo, Yoonhee; Bazarsad, Davaa; Choe, Soo Young

doi:10.12729/jbr.2012.13.2.165

Cited by 4 publications

(2 citation statements)

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“…In the present study, we investigated the time-course of 1,3-DCP-induced hepatotoxicity and the molecular mechanisms of the associated oxidative stress and apoptotic changes in rats. Our results indicate that a single oral administration Serum aminotransferase activities have long been considered sensitive indicators of hepatic injury because injury to hepatocytes alters their transport function and membrane permeability, causing leakage of the enzymes from cells (Seo et al, 2012). The marked elevation in circulating AST and ALT activities indicates severe damage to hepatocyte membranes during 1,3-DCP intoxication .…”

Section: Tablementioning

confidence: 74%

Time-course and molecular mechanism of hepatotoxicity induced by 1,3-dichloro-2-propanol in rats

Lee

et al. 2015

Environmental Toxicology and Pharmacology

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Section: Tablementioning

confidence: 74%

Time-course and molecular mechanism of hepatotoxicity induced by 1,3-dichloro-2-propanol in rats

Lee

et al. 2015

Environmental Toxicology and Pharmacology

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“…Injury to the hepatocytes alters membrane permeability and transport function, leading to leakage of serum aminotransferases [ 22 23 ]. The marked elevation of AST and ALT into the circulation indicates severe damage to hepatocyte membranes [ 5 ].…”

Section: Discussionmentioning

confidence: 99%

Role of mitogen-activated protein kinases and nuclear factor-kappa B in 1,3-dichloro-2-propanol-induced hepatic injury

Lee

et al. 2016

Lab Anim Res

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In this study, the potential hepatotoxicity of 1,3-dichloro-2-propanol and its hepatotoxic mechanisms in rats was investigated. The test chemical was administered orally to male rats at 0, 27.5, 55, and 110 mg/kg body weight. 1,3-Dichloro-2-propanol administration caused acute hepatotoxicity, as evidenced by an increase in serum aminotransferases, total cholesterol, and total bilirubin levels and a decrease in serum glucose concentration in a dose-dependent manner with corresponding histopathological changes in the hepatic tissues. The significant increase in malondialdehyde content and the significant decrease in glutathione content and antioxidant enzyme activities indicated that 1,3-dichloro-2-propanol-induced hepatic damage was mediated through oxidative stress, which caused a dose-dependent increase of hepatocellular apoptotic changes in the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assay and immunohistochemical analysis for caspase-3. The phosphorylation of mitogen-activated protein kinases caused by 1,3-dichloro-2-propanol possibly involved in hepatocellular apoptotic changes in rat liver. Furthermore, 1,3-dichloro-2-propanol induced an inflammatory response through activation of nuclear factor-kappa B signaling that coincided with the induction of pro-inflammatory mediators or cytokines in a dose-dependent manner. Taken together, these results demonstrate that hepatotoxicity may be related to oxidative stress-mediated activation of mitogen-activated protein kinases and nuclear factor-kappa B-mediated inflammatory response.

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Anti-Diabetic, Alcohol Metabolizing Enzyme, and Hepatoprotective Activity of Acer tegmentosum Maxim. Stem Extracts

Cho

Jung²,

Choi³

2015

Journal of the Korean Society of Food Science and Nutrition

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Effect of Acer tegmentosum Maxim. Extracts on Acute Hepatitis and Fatty Liver in Rats

Cited by 4 publications

References 0 publications

Time-course and molecular mechanism of hepatotoxicity induced by 1,3-dichloro-2-propanol in rats

Time-course and molecular mechanism of hepatotoxicity induced by 1,3-dichloro-2-propanol in rats

Role of mitogen-activated protein kinases and nuclear factor-kappa B in 1,3-dichloro-2-propanol-induced hepatic injury

Anti-Diabetic, Alcohol Metabolizing Enzyme, and Hepatoprotective Activity of Acer tegmentosum Maxim. Stem Extracts

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