Hydrogen Sulfide Attenuates Hypertensive Inflammation via Regulating Connexin Expression in Spontaneously Hypertensive Rats.
Hydrogen Sulfide Attenuates Hypertensive Inflammation via Regulating Connexin Expression in Spontaneously Hypertensive Rats.
复制标题
硫化氢通过调节自发性高血压大鼠的连接蛋白表达来减轻高血压炎症
DOI：
10.12659/msm.908761
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发表时间：
2018-02-27
期刊：
影响因子：
--
通讯作者：
Ma KT
中科院分区：
文献类型：
--
作者：
Ni X;Zhang L;Peng M;Shen TW;Yu XS;Shan LY;Li L;Si JQ;Li XZ;Ma KT
硫化氢（H2S）具有抗炎和抗高血压作用，而连接蛋白（Cxs）参与调节免疫稳态。本研究探讨外源性硫化氢是否通过调节自发性高血压大鼠（SHR）T淋巴细胞Cxs表达来预防高血压炎症。我们用硫氢化钠（NaHS）治疗SHR 9周。使用溶剂处理的Wistar-Kyoto大鼠（WKY）作为对照。采用尾袖法监测动脉压，压力性肌电图检查基底动脉血管功能。苏木精-伊红染色显示血管重塑和肾损伤。采用流式细胞术或ELISA法检测外周血T细胞亚群比例、T细胞亚群表面Cx40/Cx43表达及血清细胞因子水平。Western blot检测外周血淋巴细胞Cx40/Cx43蛋白表达。慢性NaHS治疗显着减轻血压升高，并抑制靶器官炎症，血管重塑和肾损伤的SHR。外源性NaHS还通过减弱KCl刺激的SHR基底动脉缩血管反应而改善血管功能。此外，慢性NaHS给药显著抑制SHR外周血炎症反应，表现为血清IL-2、IL-6和CD 4/CD 8比值降低，IL-10水平和调节性T细胞百分比升高。NaHS处理降低高血压诱导的SHR T淋巴细胞Cx40/Cx43表达。我们的数据表明，硫化氢减少高血压炎症，至少部分是由于调节T细胞亚群平衡的Cx40/Cx43表达抑制。
Hydrogen sulfide (H2S) has anti-inflammatory and anti-hypertensive effects, and connexins (Cxs) are involved in regulation of immune homeostasis. In this study, we explored whether exogenous H2S prevents hypertensive inflammation by regulating Cxs expression of T lymphocytes in spontaneously hypertensive rats (SHR). We treated SHR with sodium hydrosulfide (NaHS) for 9 weeks. Vehicle-treated Wistar-Kyoto rats (WKYs) were used as a control. The arterial pressure was monitored by the tail-cuff method, and vascular function in basilar arteries was examined by pressure myography. Hematoxylin and eosin staining was used to show vascular remodeling and renal injury. The percentage of T cell subtypes in peripheral blood, surface expressions of Cx40/Cx43 on T cell subtypes, and serum cytokines level were determined by flow cytometry or ELISA. Expression of Cx40/Cx43 proteins in peripheral blood lymphocytes was analyzed by Western blot. Chronic NaHS treatment significantly attenuated blood pressure elevation, and inhibited inflammation of target organs, vascular remodeling, and renal injury in SHR. Exogenous NaHS also improved vascular function by attenuating KCl-stimulated vasoconstrictor response in basilar arteries of SHR. In addition, chronic NaHS administration significantly suppressed inflammation of peripheral blood in SHR, as evidenced by the decreased serum levels of IL-2, IL-6, and CD4/CD8 ratio and the increased IL-10 level and percentage of regulatory T cells. NaHS treatment decreased hypertension-induced Cx40/Cx43 expressions in T lymphocytes from SHR. Our data demonstrate that H2S reduces hypertensive inflammation, at least partly due to regulation of T cell subsets balance by Cx40/Cx43 expressions inhibition.
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