Conclusions
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. 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。
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.
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).
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). Conclusions: 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. 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。