瞬时受体电位通道C与阻塞性睡眠呼吸暂停低通气综合征大鼠心脏和肾脏损害的关系

目的: 探究经典瞬时受体电位通道C（TRPC）相关蛋白在阻塞性睡眠呼吸暂停低通气综合征（OSAHS）大鼠心脏和肾脏损害中的作用。方法: 18只SD雄性大鼠随机分为实验组和对照组，每组9只。实验组大鼠在间歇性低氧舱中，每天暴露于间歇性低氧环境8 h（10:00—18:00）。此后通过实时荧光定量PCR和蛋白质印迹法分别检测大鼠心脏和肾脏组织中TRPC mRNA和相关蛋白的表达。结果: 实验组心脏组织中TRPC3、TRPC4、TRPC5的mRNA表达较对照组升高（均P < 0.05），而肾脏组织TRPC1、TRPC3、TRPC4、TRPC5、TRPC6、TRPC7的mRNA表达在两组之间差异无统计学意义（均P>0.05）；实验组肾脏组织中TRPC4、TRPC5、TRPC6的mRNA表达低于心脏组织（均P < 0.05），对照组肾脏组织TRPC7的mRNA表达高于心脏组织（P < 0.05）。实验组心脏组织中的TRPC5蛋白表达较对照组升高（P < 0.05），而肾脏组织TRPC5、TRPC6、TRPC7相关蛋白的表达在两组之间差异无统计学意义（均P>0.05）。结论: TRPC5可能参与OSAHS心脏损害的病理生理过程，有望成为治疗OSAHS所致心脏损害的药物新靶点。

Correlation between transient receptor potential canonical channel with heart and kidney injure of rat model of obstructive sleep apnea hypopnea syndrome

Objective: To investigate the expression of transient receptor potential canonical channels (TRPCs) in the heart and kidney of rat model of obstructive sleep apnea hypopnea syndrome (OSAHS). Methods: Eighteen male SD rats were randomly assigned to intermittent hypoxia (IH) group (n=9) and control group (n=9). In IH group, rats were placed in a chamber and exposed to intermittent hypoxia for 8h (10AM-6PM) daily. The expression of TRPC-related mRNA and protein in the heart and kidney tissue were detected by qRT-PCR and Western blotting, respectively. Results: The mRNA expressions of TRPC3/TRPC4/TRPC5 in heart tissues of IH group were increased significantly compared with the control group (all P>0.05); while there were no significant differences in the mRNA expressions of TRPC1/TRPC3/TRPC4/TRPC5/TRPC6/TRPC7 in kidney tissue between two groups (all P < 0.05). The mRNA expressions of TRPC4, TRPC5 and TRPC6 in kidney tissues of IH group were lower than that in heart tissues (all P < 0.05). The mRNA expression of TRPC7 in kidney tissues of control group was significantly higher than that in heart tissues (P < 0.05). The expression of TRPC5 protein in heart tissues of IH group was significantly higher than that in the control group (P < 0.05); while there was no significant differences in the expression of TRPC5/TRPC6/TRPC7 protein in kidney tissue between two groups (all P>0.05). Conclusion: The IH rat model shows that TRPC5 channel is likely to be involved in the OSAHS induced pathophysiological changes in the myocardium and may become a target to prevent OSAHS related cardiac damage.