NDLI: Upregulation of heat shock protein 32 with hemin alleviates acute heat-induced hepatic injury in mice

Content Provider	Springer Nature Link
Author	Li, Cheng min Li, Lian Wu, Jie Bai, Jing yan Sun, Yu Huang, Shuai Wang, Gen lin
Copyright Year	2014
Abstract	Heat shock protein 32 (HSP32) is a stress response protein that can be induced by heat stress in the liver, and its induction can act as an important cellular defence mechanism against heat-induced liver injury. To investigate the functional role of HSP32 in protecting liver tissue against heat stress in mice and the mechanism by which it achieves this protective effect, HSP32 expression and carbon monoxide (CO) contents in a model of mice subjected to acute, transient heat exposure were examined. Furthermore, functional and histological parameters of liver damage and the possible involvement of oxidative stress to induce oxidative deterioration of liver functions and caspase-3 expression were also investigated in this study. We found that heat treatment of mice produced severe hepatic injury, whereas upregulation of HSP32 with hemin pretreatment prevented mice from liver damage. In contrast, addition of Sn-protoporphyrin (SnPP) to inhibit HSP32 expression completely reversed its hepatoprotective effect. It is concluded that upregulation of HSP32 by hemin could alleviate acute heat-induced hepatocellular damage in mice, and its by-product CO seems to play a more important role in hepatoprotective mechanism.
Starting Page	675
Ending Page	683
Page Count	9
File Format	PDF
ISSN	13558145
Journal	Cell Stress and Chaperones
Volume Number	19
Issue Number	5
e-ISSN	14661268
Language	English
Publisher	Springer Netherlands
Publisher Date	2014-01-29
Publisher Place	Dordrecht
Access Restriction	Subscribed
Subject Keyword	HSP32 Liver injury Acute heat stress Caspase-3 Hemin Biomedicine general Cell Biology Biochemistry Immunology Cancer Research Neurosciences
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry

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