Schisandra Chinensis Baillon regulates the gene expression of phase II antioxidant/detoxifying enzymes in hepatic damage induced rats.
- Author:
Han I JANG
1
;
Gyeong Min DO
;
Hye Min LEE
;
Hyang Mok OK
;
Jae Ho SHIN
;
Oran KWON
Author Information
- Publication Type:Original Article
- Keywords: Schisandra chinensis baillon; Tert-butyl hydroperoxide; endogenous antioxidant capacity; hepatotoxicity
- MeSH: Animals; Catalytic Domain; Erythrocytes; Gene Expression*; Glutamate-Cysteine Ligase; Glutathione; Glutathione Peroxidase; Glutathione Reductase; Glutathione Transferase; Hand; Incidence; Liver; Necrosis; Neutrophil Infiltration; Rats*; Rats, Sprague-Dawley; Schisandra*; tert-Butylhydroperoxide
- From:Nutrition Research and Practice 2014;8(3):272-277
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND/OBJECTIVES: This study investigated the antioxidant activities and hepatoprotective effects of Schisandra chinensis Baillon extract (SCE) against tert-butyl hydroperoxide (t-BHP)-induced oxidative hepatic damage in rats. MATERIALS/METHODS: Sprague-Dawley (SD) rats were pretreated with SCE (300, 600, and 1,200 mg/kg BW) or saline once daily for 14 consecutive days. On day 14, each animal, except those belonging to the normal control group, were injected with t-BHP (0.8 mmol/kg BW/i.p.), and all of the rats were sacrificed 16 h after t-BHP injection. RESULTS: Although no significant differences in AST and ALT levels were observed among the TC and SCE groups, the high-dose SCE group showed a decreasing tendency compared to the TC group. However, erythrocyte SOD activity showed a significant increase in the low-dose SCE group compared with the TC group. On the other hand, no significant differences in hepatic total glutathione (GSH) level, glutathione reductase (GR), and glutathione peroxidase (GSH-Px) activities were observed among the TC and SCE groups. Hepatic histopathological evaluation revealed that pretreatment with SCE resulted in reduced t-BHP-induced incidence of lesions, such as neutrophil infiltration, swelling of liver cells, and necrosis. In particular, treatment with a high dose of SCE resulted in induction of phase II antioxidant/detoxifying enzyme expression, such as glutathione S-transferase (GST) and glutamate-cysteine ligase catalytic subunit (GCLC). CONCLUSIONS: Based on these results, we conclude that SCE exerts protective effects against t-BHP induced oxidative hepatic damage through the reduction of neutrophil infiltration, swelling of liver cells, and necrosis. In addition, SCE regulates the gene expression of phase II antioxidant/detoxifying enzymes independent of hepatic antioxidant enzyme activity.
