阿司匹林诱导的热休克蛋白B1对鸡心肌细胞热应激损伤的体外评价
In vitro evaluation of aspirin-induced HspB1 against heat stress damage in chicken myocardial cells.
作者信息
Wu Di, Zhang Miao, Xu Jiao, Song Erbao, Lv Yinjun, Tang Shu, Zhang Xiaohui, Kemper N, Hartung J, Bao Endong
机构信息
College of Veterinary Medicine, Nanjing Agricultural University, Weigang 1, Nanjing, 210095, China.
College of Animal Science and Technology, Jinling Institute of Technology, Nanjing, 210038, China.
出版信息
Cell Stress Chaperones. 2016 May;21(3):405-13. doi: 10.1007/s12192-016-0666-8. Epub 2016 Feb 24.
To understand the potential association of heat stress resistance with HspB1 induction by aspirin (ASA) in chicken myocardial cells, variations of HspB1 expression and heat stressed-induced damage of myocardial cells after ASA administration were studied in primary cultured myocardial cells. Cytopathological lesions as well as damage-related enzymes, such as creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH), indicated the considerable protective ability of ASA pre-treatment against acute heat stress. Immunostaining assays showed that heat stress caused HspB1 to relocate into the nucleus, while ASA did not. ELISA analysis, revealed that HspB1 expression induced by ASA averaged 45.62-fold higher than that of the control. These results indicated that the acute heat-stressed injuries were accompanied by comparatively lower HspB1 expression caused by heat stress in vitro. ASA pre-treatment induced a level of HspB1 presumed to be sufficient to protect myocardial cells from acute heat stress in the extracorporal model, although more detailed mechanisms will require further investigation.
为了解阿司匹林（ASA）诱导的HspB1与鸡心肌细胞耐热应激之间的潜在关联，我们在原代培养的心肌细胞中研究了ASA给药后HspB1表达的变化以及热应激诱导的心肌细胞损伤。细胞病理学损伤以及与损伤相关的酶，如肌酸激酶-MB（CK-MB）和乳酸脱氢酶（LDH），表明ASA预处理对急性热应激具有显著的保护能力。免疫染色分析表明，热应激导致HspB1重新定位到细胞核中，而ASA则不会。ELISA分析显示，ASA诱导的HspB1表达平均比对照组高45.62倍。这些结果表明，在体外，急性热应激损伤伴随着热应激导致的相对较低的HspB1表达。尽管更详细的机制需要进一步研究，但在体外模型中，ASA预处理诱导的HspB1水平被认为足以保护心肌细胞免受急性热应激。
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