七氟醚和缺氧预适应诱导乳鼠心肌细胞HSP—70表达的改变

目的：探讨七氟醚预适应和缺氧预适应对乳鼠心肌细胞热休克蛋白70表达的影响。方法：第2代培养心肌细胞随机分为正常对照组(C组)、缺氧/复氧组(A／R组)、缺氧预适应组(IP组)和七氟醚预适应组(S组)，每组均缺氧2h，复氧48h。分别取复氧0，1，12，24，36和48h的细胞，用免疫组化染色检测HSP70表达并进行图象分析。结果：在各个时间点，S组和IP组间的HSP70表达均显著高于A／R组和C组(P＜0．01)，A／R组的HSP70表达略高于C组，S组和IP组间的HSP70表达差异无显著性(P＞0．05)。随着复氧时间的延长，S组和IP组间的HSP70表达从1h开始增加，24h表达最强，与1h相比差异具有显著性(P＜0．05)。结论：七氟醚预处理和缺氧预处理均可诱导乳鼠心肌细胞HSP70在延迟相呈高表达，提示HSP70参与了七氟醚预适应和缺氧预适应的延迟保护相。

Effects of sevoflurane-induced and anoxia-induced preconditioning on HSP70 expression in neonatal rat cardiomyocytes]

OBJECTIVE: To explore the effects of sevoflurane-preconditioning and anoxia-preconditioning on HSP70 expression in neonatal rat cardiomyocytes. METHODS: The second generation of primary cultured cardiomyocytes was randomly divided into 4 groups: normal control (Group C), anoxia/reoxygenation group (Group A/R), anoxia-preconditioning group (Group IP), and sevoflurane-preconditioning group (Group S); In each group, the cardiomyocytes were subjected to anoxia (2 h) followed by reoxygenation (48 h). The immunohistochemistry was used to determine the expression of HSP70 protein in neonatal rat cardiomyocytes at 0, 1, 12, 24, 36 and 48 h after reoxygenation respectively. RESULTS: At each point of time studying reoxygenation, the expression level of HSP70 in Group S and Group IP was significantly higher than that in Group A/R and Group C (P < 0.01). The HSP70 expression level in Group A/R was slightly higher than that in Group C. No significant difference was found in HSP70 expression between Group IP and Group S (P > 0.05). The expression level of HSP70 protein in both Group S and Group IP increased concomitantly with the reoxygenation time from 1 h after reoxygenation, and reached the peak at 24 h of reoxygenation (P < 0.01). CONCLUSION: sevoflurane-preconditioning and anoxia preconditioning can induce the high level expression of HSP70 in the neonatal rat cardiomyocytes with the phase of protection delayed. It is suggested that HSP70 may be involved in the process of the delayed phase of protection induced by sevoflurane-preconditioning and anoxia-preconditioning respectively.