Yang Yang1, Zhiliang Chen2, Lvyu Deng1, Juan Yu2, Kai Wang1, Xing Zhang1, Guang Ji1, Fenghua Li3. 1. Experiment Center For Science and Technology, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, People's Republic of China. 2. Fujian Provincial Key Laboratory of Pien Tze Huang Natural Medicine Research and Development, Zhangzhou Pien Tze Huang Pharmaceutical CO., LTD., Fujiian 363000, People's Republic of China. 3. Experiment Center For Science and Technology, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, People's Republic of China. Electronic address: lfh05@outlook.com.
Abstract
OBJECTIVE: To explore whether Pien Tze Huang (PTH) exerts a hepatoprotective effect via inhibiting the PERK/eIF2ɑ signaling pathway using an experimental animal model of alcoholic and high-fat diet rats. METHODS: A liver injury rat model was established and treated with PTH. Pathological changes in the liver were evaluated by hematoxylin and eosin staining. Hepatic biochemical indexes were detected using an automatic biochemical analyzer. The level of Hcy in serum samples was analyzed using an ELISA. Levels of mRNAs related to ER stress signaling were measured by real-time quantitative-PCR, and protein expression levels were measured by Western blot analysis. RESULTS: PTH ameliorated the defects in hepatic function, hepatic pathology and the impairment in lipid metabolism observed in the alcoholic and high-fat diet rats. Moreover, PTH reduced the serum Hcy level and inhibited the PERK/eIF2ɑ pathway in response to ER stress. CONCLUSIONS: These results suggest that the administration of PTH ameliorated the severity of alcoholic and high-fat diet rats possibly by inhibiting the Hcy-induced PERK/eIF2α pathway.
OBJECTIVE: To explore whether Pien Tze Huang (PTH) exerts a hepatoprotective effect via inhibiting the PERK/eIF2ɑ signaling pathway using an experimental animal model of alcoholic and high-fat diet rats. METHODS: A liver injuryrat model was established and treated with PTH. Pathological changes in the liver were evaluated by hematoxylin and eosin staining. Hepatic biochemical indexes were detected using an automatic biochemical analyzer. The level of Hcy in serum samples was analyzed using an ELISA. Levels of mRNAs related to ER stress signaling were measured by real-time quantitative-PCR, and protein expression levels were measured by Western blot analysis. RESULTS: PTH ameliorated the defects in hepatic function, hepatic pathology and the impairment in lipid metabolism observed in the alcoholic and high-fat diet rats. Moreover, PTH reduced the serum Hcy level and inhibited the PERK/eIF2ɑ pathway in response to ER stress. CONCLUSIONS: These results suggest that the administration of PTH ameliorated the severity of alcoholic and high-fat diet rats possibly by inhibiting the Hcy-induced PERK/eIF2α pathway.