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片仔癀通过抑制酒精和高脂饮食大鼠的PERK/eIF2α信号通路改善肝损伤。

Pien Tze Huang ameliorates liver injury by inhibiting the PERK/eIF2α signaling pathway in alcohol and high-fat diet rats.

作者信息

Yang Yang, Chen Zhiliang, Deng Lvyu, Yu Juan, Wang Kai, Zhang Xing, Ji Guang, Li Fenghua

机构信息

Experiment Center For Science and Technology, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, People's Republic of China.

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.

出版信息

Acta Histochem. 2018 Aug;120(6):578-585. doi: 10.1016/j.acthis.2018.06.006. Epub 2018 Jul 10.

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.

摘要

目的

使用酒精性和高脂饮食大鼠实验动物模型,探讨片仔癀(PTH)是否通过抑制PERK/eIF2ɑ信号通路发挥肝保护作用。

方法

建立肝损伤大鼠模型并用PTH治疗。通过苏木精和伊红染色评估肝脏的病理变化。使用自动生化分析仪检测肝脏生化指标。使用酶联免疫吸附测定法分析血清样本中的同型半胱氨酸(Hcy)水平。通过实时定量聚合酶链反应测量与内质网应激信号相关的mRNA水平,通过蛋白质免疫印迹分析测量蛋白质表达水平。

结果

PTH改善了酒精性和高脂饮食大鼠的肝功能缺陷、肝脏病理以及脂质代谢损伤。此外,PTH降低了血清Hcy水平,并在应对内质网应激时抑制了PERK/eIF2ɑ通路。

结论

这些结果表明,给予PTH可能通过抑制Hcy诱导的PERK/eIF2α通路减轻了酒精性和高脂饮食大鼠的严重程度。

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