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

Male Mice, Inbred BALB C 0303 health sciences Hot Temperature Alanine Transaminase Apoptosis Cytochrome P-450 CYP2E1 Heat Stress Disorders Mice Necrosis 03 medical and health sciences Liver Cytochrome P-450 CYP1A2 Proliferating Cell Nuclear Antigen Hepatocytes In Situ Nick-End Labeling Animals Cytochrome P-450 CYP3A Female HSP70 Heat-Shock Proteins Aspartate Aminotransferases Cell Proliferation
DOI: 10.1007/s12576-011-0183-6 Publication Date: 2011-11-28T08:31:19Z
ABSTRACT
Heat stress will stimulate cells of living organisms to generate heat shock proteins (Hsps). In the mouse liver, impacts on hepatocyte proliferation, apoptosis and metabolism have not been studied systematically at different temperatures. this research, test mice were heated 40, 42, 44 46°C, respectively, for 20 min recovered room temperature 8 h in normal feeding conditions; control animals kept without stress. The expression levels Hsp70, Pcna, Bax, Bcl2, cytochrome P450 1A2 (CYP1A2), CYP2E1 analog CYP3A4 (not reported before), parameters reflecting strength, cell metabolism, detected by western blotting, immunohistochemistry semi-quantitative RT-PCR mice. Haematoxylin-eosin (H&E) staining TUNEL analysis further used study temperatures hepatocellular necrosis apoptosis. Serum AST ALT levels, markers liver injury, measured after data show that Hsp70 was significantly increased when (P < 0.05). At lower (40 or 42°C), CYP1A2 considerably 0.05) while induced > higher (44 46°C), Pcna decreased Expressions especially 46°C Expression could be increase 40°C but high between they than those 42 0.05), 0.01). conclusion, promotes proliferation improves metabolic efficiency inhibits induces necrosis. This may give a hint understanding human injury Moreover, it is first time cytoplasm. It worthwhile dissect its function future work.
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