Wen Wen, Yao Qiaoling, Chen Yulan, Li Zhiqiang, Sun Xiaojing, Li Yu, Zhang Junshi, Simayi Zhulipiya, Xu Xinjuan
Department of Hypertension, the First Affiliated Hospital of Xinjiang Medical University, Urumqi 830011, China.
Department of Physiology, Preclinical Medicine Collage of Xinjiang Medical University, Urumqi 830054, China.
Zhejiang Da Xue Xue Bao Yi Xue Ban. 2020 Aug 25;49(4):439-446. doi: 10.3785/j.issn.1008-9292.2020.04.16.
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).
Eighteen male SD rats were randomly assigned to intermittent hypoxia (IH) group (=9 ) and control group (=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.
The mRNA expressions of TRPC3/TRPC4/TRPC5 in heart tissues of IH group were increased significantly compared with the control group (all >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 <0.05). The mRNA expressions of TRPC4, TRPC5 and TRPC6 in kidney tissues of IH group were lower than that in heart tissues (all <0.05). The mRNA expression of TRPC7 in kidney tissues of control group was significantly higher than that in heart tissues (<0.05). The expression of TRPC5 protein in heart tissues of IH group was significantly higher than that in the control group (<0.05); while there was no significant differences in the expression of TRPC5/TRPC6/TRPC7 protein in kidney tissue between two groups (all >0.05).
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.
探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)大鼠模型心脏和肾脏中瞬时受体电位香草酸亚家族(TRPCs)的表达。
将18只雄性SD大鼠随机分为间歇性缺氧(IH)组(n = 9)和对照组(n = 9)。IH组大鼠置于舱内,每天暴露于间歇性缺氧环境8小时(上午10点至下午6点)。分别采用qRT-PCR和蛋白质免疫印迹法检测心脏和肾脏组织中TRPC相关mRNA和蛋白的表达。
与对照组相比,IH组心脏组织中TRPC3/TRPC4/TRPC5的mRNA表达显著增加(均P>0.05);而两组肾脏组织中TRPC1/TRPC3/TRPC4/TRPC5/TRPC6/TRPC7的mRNA表达无显著差异(均P<0.05)。IH组肾脏组织中TRPC4、TRPC5和TRPC6的mRNA表达低于心脏组织(均P<0.05)。对照组肾脏组织中TRPC7的mRNA表达显著高于心脏组织(P<0.05)。IH组心脏组织中TRPC5蛋白的表达显著高于对照组(P<0.05);而两组肾脏组织中TRPC5/TRPC6/TRPC7蛋白的表达无显著差异(均P>0.05)。
IH大鼠模型表明,TRPC5通道可能参与了OSAHS诱导的心肌病理生理变化,可能成为预防OSAHS相关心脏损伤的靶点。