新疆哈萨克族高血压病患者淋巴细胞KCa3.1及CaN-NFAT信号通路的变化

摘要

目的:研究新疆高高敏C反应蛋白(hsCRP)水平哈萨克族高血压患者外周血淋巴细胞钙调神经磷酸酶/活化T细胞核因子(CaN/NFAT)信号通路及其钙激活钾通道(KCa3.1)表达发生的变化,探讨淋巴细胞钾通道参与高血压病炎症反应的机制.方法:选择2014年2月至2014年11月在我院心脏中心首诊,未经降压治疗的新疆哈萨克族高血压患者.根据检测的hsCRP水平,选择hsCRP水平≥3mg/L的患者50例为高hsCRP组,hsCRP水平<3mg/L的患者50例为正常hsCRP组.检测比较两组KCa3.1、肿瘤坏死因子(TNF)-α基因、蛋白表达水平,以及淋巴细胞CaN、NFAT活性.结果:与正常hsCRP组比较,高hsCRP组淋巴细胞KCa3.1 mRNA[(0.86±0.16)比(2.48±0.22)]、TNF-α mRNA[(1.02±0.15)比(2.90±0.13)]、KCa3.1 蛋白[(1.00±0.02)比(2.46±0.04)]、TNF-α 蛋白[(1.01±0.02)比(2.04±0.06)]表达水平、CaN活性[(1.04±0.15)比(2.83±0.08)]、NFAT活性[(0.96±0.06)比(2.65±0.07)]均显著升高,P均<0.01.结论:具有炎症反应的新疆哈萨克族高血压患者外周血淋巴细胞上KCa3.1及CaN-NFAT信号通路表达增加,提示淋巴细胞KCa3.1可能通过CaN/NFAT信号通路参与高血压病的发生发展.%Objective: To study changes of peripheral blood lymphocyte calcineurin/ nuclear factor of activated T cells (CaN/NFAT) signaling pathway and calcium activated potassium channel (KCa3.1) expression in Kazak hypertensive patients with high high sensitive C reactive protein (hsCRP) level from Xinjiang, and explore the mechanism of lymphocyte potassium channel involving in inflammation of hypertension.Methods: Kazak hypertensive patients from Xinjiang, who were first diagnosed in our heart center without antihypertensive therapy from Feb 2014 to Nov 2014, were selected.According to detected hsCRP level, a total of 50 hsCRP≥3mg/L patients were enrolled as high hsCRP group, and 50 hsCRP<3mg/L patients were enrolled as normal hsCRP group.Gene and protein expression levels of KCa3.1 and tumor necrosis factor (TNF)-α, and activities of lymphocyte CaN and NFAT were measured and compared between two groups.Results: Compared with normal hsCRP group, there were significant rise in expression levels of lymphocyte KCa3.1 mRNA [(0.86±0.16) vs.(2.48±0.22)], TNF-α mRNA [(1.02±0.15) vs.(2.90±0.13)], KCa3.1 protein [(1.00±0.02) vs.(2.46±0.04)] and TNF-α protein [(1.01±0.02) vs.(2.04±0.06)], and activities of CaN [(1.04±0.15) vs.(2.83±0.08)] and NFAT [(0.96±0.06) vs.(2.65±0.07)] in high hsCRP group, P<0.01 all.Conclusion: In Kazak hypertensive patients with inflammatory reaction from Xinjiang, KCa3.1 and CaN-NFAT signaling pathway expression rises, suggesting that lymphocyte KCa3.1 may be involved in occurrence and development of hypertension via CaN/NFAT signaling pathway.