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本研究探讨热休克反应（ｈｅａｔｓｈｏｃｋｒｅｓｐｏｎｓｅ，ＨｓＲ）对抗过氧化氢（Ｈ２Ｏ２）所致牛肺动脉内皮细胞（ＢＰＡＥＣｓ）损伤的保护作用及机制。实验发现，预先热休克处理（４２℃，２ｈ）可使ＢＰＡＥＣｓ中热休克蛋白７０ｋＤａ（ＨＳＰ７０）及ＨＳＰ７０ｍＲＮＡ明显增多，同时显著减轻Ｈ２Ｏ２所致的ＢＰＡＥＣｓ中乳酸脱氢酶释放和硫代巴比妥酸反应物含量增加及过氧化氢酶和超氧化物歧化酶活性的降低等变化。进一步实验证明放线菌酮和放线菌素Ｄ能分别抑制热休克诱导的Ｈ８Ｐ７０和ＨＳＰ７０ｍＲＮＡ的增多，同时均能取消ＨＳＲ对抗Ｈ２Ｏ２所致ＢＰＡＥＣｓ损伤的保护作用。结果提示，ＨＳＲ具有对抗Ｈ２Ｏ２所致ＢＰＡＥＣｓ损伤的保护作用；此种保护作用与细胞经热休克处理后细胞中热休克基因在转录和翻译两个水平的表达增强及抗氧化能力增加有关。
This study was aimed to investigate the protective effect and mechanism of heat shock response (HsR) against hydrogen peroxide (H2O2) -induced bovine pulmonary artery endothelial cells (BPAECs) injury. The results showed that pre-heat shock treatment (42 ℃, 2h) can significantly increase the heat shock protein 70kDa (HSP70) and HSP70mRNA in BPAECs, and significantly reduce the release of lactate dehydrogenase and thiobarbituric acid in BPAECs induced by H2O2 Reactant content and catalase and superoxide dismutase activity decreased. Further experiments showed that cycloheximide and actinomycin D could inhibit heat shock-induced increase of H8P70 and HSP70mRNA respectively, and both could abolish the protective effect of HSR against H2O2-induced BPAECs injury. The results suggest that HSR possesses the protective effect against BPAECs injury induced by H2O2. This protective effect is related to the enhanced expression of heat shock genes at the transcriptional and translational levels and the anti-oxidative capacity of cells after heat shock treatment.