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In vitro evaluation of aspirin-induced HspB1 against heat stress damage in chicken myocardial cells

机译:阿司匹林诱导的HspB1对鸡心肌细胞热应激损伤的体外评价

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摘要

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.
机译:为了解鸡心肌细胞中热应激抗性与阿司匹林(ASA)诱导HspB1诱导的潜在联系,研究了ASA给药后原代培养的心肌细胞中HspB1表达的变化和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,例如肌酸激酶-MB(CK-MB)和乳酸脱氢酶(LDH),表明ASA预处理对急性热应激具有相当大的保护能力。免疫染色试验表明,热应激导致HspB1重新定位到细胞核中,而ASA没有。 ELISA分析显示,ASA诱导的HspB1表达平均比对照高45.62倍。这些结果表明,急性热应激损伤伴随着由体外热应激引起的HspB1表达相对较低。 ASA预处理诱导的HspB1水平被认为足以保护心肌细胞免受体外模型中的急性热应激,尽管更详细的机制尚需进一步研究。

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