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目的:探讨替普瑞酮(GGA)诱导的热休克蛋白70(HSP70)在香烟提取物(CSE)引起的气道平滑肌细胞(ASMCs)凋亡中对C-Jun N-terminal激酶(JNKs)的影响。方法:在体外培养Wistar大鼠的气道平滑肌细胞中,给予GGA处理前后,给予CSE刺激3 h。用流式细胞仪(FCM)检测细胞凋亡情况,Western blot的方法检测HSP70和p-JNK的表达。结果:CSE诱导ASMCs凋亡随CSE浓度的增加而逐渐增加,两者相比有显著性差异(P<0.05);GGA预处理后再加入不同浓度的CSE处理的气道平滑肌细胞的凋亡较单纯CSE组相比有显著性差异(P<0.05)。在给予CSE刺激后,各组中的HSP70的表达较对照组有明显的降低,而且随CSE浓度越高降低越明显(P<0.05);p-JNK的表达随CSE浓度的增高而增多(P<0.05)。GGA预处理后的各组细胞的HSP70的表达与对照组比较有明显的增多(P<0.05)。在给予GGA预处理后,再加入CSE处理的气道平滑肌细胞中,与对照组比较HSP70的表达有所降低但无显著差异,p-JNK的表达在GGA+CSE组中的表达较单纯CSE组中有所下降(P<0.05)。结论:较高浓度的CSE能引起气道平滑肌细胞的凋亡并且伴随p-JNK的表达的增多。GGA处理气道平滑肌细胞后引起HSP70表达的增加,并且抑制较高浓度CSE所致的平滑肌细胞的凋亡,这可能与HSP70下调p-JNK的活性有关。
AIM: To investigate the effect of heat shock protein 70 (HSP70) induced by teprenone (GGA) on C-Jun N-terminal kinase (JNKs) in airway smooth muscle cells (ASMCs) influences. Methods: The airway smooth muscle cells of Wistar rats were cultured for 3 h before and after GGA treatment. Cell apoptosis was detected by flow cytometry (FCM), and Western blot was used to detect the expression of HSP70 and p-JNK. Results: The apoptosis of ASMCs induced by CSE increased gradually with the increase of CSE concentration (P <0.05). Compared with the CSE-treated CSE, the apoptosis of airway smooth muscle cells treated with different concentrations of CSE Compared with CSE group, there was significant difference (P <0.05). After CSE stimulation, the expression of HSP70 in each group was significantly lower than that in control group (P <0.05); the expression of p-JNK increased with the increase of CSE concentration (P <0.05). The expression of HSP70 in each group after GGA pretreatment was significantly increased compared with the control group (P <0.05). Compared with the control group, the expression of HSP70 in GAS preconditioning group and CSE-treated group was lower than that in control group, but there was no significant difference. The expression of p-JNK in GGA + CSE group was higher than that in CSE group (P <0.05). CONCLUSIONS: Higher concentration of CSE can induce apoptosis of airway smooth muscle cells with the accompanying increase of p-JNK expression. GGA treatment resulted in the increase of HSP70 expression in airway smooth muscle cells and the inhibition of CSE-induced apoptosis in smooth muscle cells, which may be related to the down-regulation of p-JNK activity by HSP70.