Systematical analysis of impacts of heat stress on the proliferation, apoptosis and metabolism of mouse hepatocyte

作者：Sanqiang Li, Ruifang Li, Ruifang Li, Shoumin Xi, Shu Hu, Zhi-Qiang Jia, Shao-Ping Li, Shao-Ping Li, Xinli Wen, Yakun Song, Shuai Li, Shuai Li, Shipeng Li, Shipeng Li, Fei-Biao Wei, Xueliang Chen · 发表于：The Journal of Physiological Sciences · 年份：2011 · DOI：10.1007/s12576-011-0183-6 · 被引用次数：33 · 研究领域：Liver Disease Diagnosis and Treatment、Heat shock proteins research、Adipose Tissue and Metabolism

Heat stress will stimulate cells of living organisms to generate heat shock proteins (Hsps). In the mouse liver, impacts of heat stress on hepatocyte proliferation, apoptosis and metabolism have not been studied systematically at different temperatures. In this research, the test mice were heated to 40, 42, 44 and 46°C, respectively, for 20 min and recovered at room temperature for 8 h in normal feeding conditions; the control animals were kept at room temperature without heat stress. The expression levels of Hsp70, Pcna, Bax, Bcl2, cytochrome P450 1A2 (CYP1A2), CYP2E1 and analog of CYP3A4 (not reported in mouse before), the parameters reflecting stress strength, cell proliferation, apoptosis and metabolism, were detected by western blotting, immunohistochemistry and semi-quantitative RT-PCR in test and control mice. Haematoxylin-eosin (H&E) staining and TUNEL analysis were further used to study the impacts of heat stress at different temperatures on hepatocellular necrosis and apoptosis. Serum AST and ALT levels, the markers of liver injury, were measured after heat stress at different temperatures. The data show that Hsp70 expression was significantly increased when temperature increased (P < 0.05). At lower temperatures (40 or 42°C), expression of Pcna, CYP1A2 and analog of CYP3A4 were considerably increased (P < 0.05) while hepatocyte necrosis and apoptosis were not induced (P > 0.05). At higher temperatures (44 or 46°C), expression of Pcna was decreased while hepatocyte ...