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抑制 Rho/ROCK 信号通路参与运动训练对自发性高血压大鼠心脏的保护作用。

Inhibition of Rho/ROCK signaling pathway participates in the cardiac protection of exercise training in spontaneously hypertensive rats.

机构信息

Department of Physiology, School of Basic Medical Sciences, Hebei University, 342 Yu Hu Dong Rd., Baoding, 071000, People's Republic of China.

Clinical School of Medicine, Hebei University, Baoding, 071000, People's Republic of China.

出版信息

Sci Rep. 2022 Oct 25;12(1):17903. doi: 10.1038/s41598-022-22191-3.

DOI:10.1038/s41598-022-22191-3
PMID:36284153
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9596711/
Abstract

Exercise training (ExT) is capable of improving the heart function of spontaneously hypertensive rats (SHRs), but the underlying molecular mechanisms remain elusive. This study was aimed to investigate whether inhibition of RhoA/ROCK signaling pathway contributes to the cardiac protection by low-intensity ExT in SHRs. The results demonstrated that, compared with Wistar-Kyoto (WKY) rats, SHRs obviously exhibited higher blood pressure, increased heart weight index and thickness of left ventricular wall, decreased left ventricular function, damaged myocardial construction, and increased collagen fiber of left ventricle (P < 0.05 or P < 0.01). Meanwhile, the mRNA and protein expression levels of RhoA and ROCK in the heart of SHRs were significantly increased, compared with those of WKY rats (P < 0.05 or P < 0.01). Interestingly, the pathological changes of heart aforementioned were all improved in SHR-ExT rats compared with SHR-Sed rats (P < 0.05 or P < 0.01), indicating the cardiac protection of exercise training. In addition, the cardiac protective effect of exercise training could be blocked by LPA, an activator of Rho/ROCK signaling, and the protective effect in SHR rats could be mimicked by Fasudil, an inhibitor of Rho/ROCK signaling. The results strongly suggest that low-intensity ExT can protect heart against structure and function through inhibiting Rho/ROCK signaling pathway in hypertensive rats.

摘要

运动训练（ExT）能够改善自发性高血压大鼠（SHRs）的心脏功能，但潜在的分子机制仍不清楚。本研究旨在探讨 RhoA/ROCK 信号通路的抑制是否有助于低强度 ExT 对 SHR 心脏的保护作用。结果表明，与 Wistar-Kyoto（WKY）大鼠相比，SHRs 血压明显升高，左心室壁厚度和左心室重量指数增加，左心室功能降低，心肌结构受损，左心室胶原纤维增加（P<0.05 或 P<0.01）。同时，与 WKY 大鼠相比，SHRs 心脏中 RhoA 和 ROCK 的 mRNA 和蛋白表达水平明显升高（P<0.05 或 P<0.01）。有趣的是，与 SHR-Sed 大鼠相比，SHR-ExT 大鼠的上述心脏病理变化均有所改善（P<0.05 或 P<0.01），表明运动训练具有心脏保护作用。此外，Rho/ROCK 信号的激活剂 LPA 可阻断运动训练的心脏保护作用，Rho/ROCK 信号的抑制剂 Fasudil 可模拟 SHR 大鼠的保护作用。这些结果强烈表明，低强度 ExT 通过抑制高血压大鼠的 Rho/ROCK 信号通路可以保护心脏的结构和功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bb1/9596711/603d439a4e01/41598_2022_22191_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bb1/9596711/44225c124882/41598_2022_22191_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bb1/9596711/9c7f6809c477/41598_2022_22191_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bb1/9596711/694457ceefbd/41598_2022_22191_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bb1/9596711/4444a77e0dfa/41598_2022_22191_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bb1/9596711/ee05a1a62209/41598_2022_22191_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bb1/9596711/603d439a4e01/41598_2022_22191_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bb1/9596711/44225c124882/41598_2022_22191_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bb1/9596711/9c7f6809c477/41598_2022_22191_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bb1/9596711/694457ceefbd/41598_2022_22191_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bb1/9596711/4444a77e0dfa/41598_2022_22191_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bb1/9596711/ee05a1a62209/41598_2022_22191_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bb1/9596711/603d439a4e01/41598_2022_22191_Fig6_HTML.jpg

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