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目的观察高盐饮食对Wistar大鼠心肌重构的影响,探讨替米沙坦逆转左心室重构的可能机制。方法49只Wistar大鼠经高盐饲养后随机分为高盐高血压组[n=12,NaCl约2.015g/(只·d)]和高盐正常血压组[n=12,NaCl约2.015g/(只·d)],同时设立对照组[n=13,NaCl约0.094g/(只·d)]和替米沙坦组[n=12,NaCl约1.966g/(只·d)]。采用HE和Masson染色观察心肌组织形态和结构变化。生化酶学法测定血液及左心室中超氧化物歧化酶(SOD)活性和丙二醛浓度,酶联免疫吸附试验(ELISA)测定血清高敏C反应蛋白(hsCRP)浓度,放射免疫法测定心肌肿瘤坏死因子α(TNF-α)浓度,Western blot法检测心肌核转录因子κB(NF-κB)p65蛋白表达水平。结果与对照组比较,高盐两组左心室质量指数(LVMI)、心肌细胞直径(CMD)、心肌间纤维化面积(MIFI)、hsCRP、左心室TNF-α浓度、NF-κB p65蛋白表达水平及血清SOD活性明显升高(均P<0.05),但左心室SOD活性降低;心肌重构(LVMI、CMD、MIFI)与左心室SOD活性呈负相关[分别r=-0.448、-0.625、-0.492,均P<0.05],与NF-κB蛋白表达水平呈正相关[r=0.556、0.693、0.803,均P<0.05];替米沙坦能改善高盐诱导的左心室重构,并增强左心室SOD活性[替米沙坦组(72.20±12.17)比高盐高血压组(58.34±5.78)、高盐正常血压组(54.59±6.65)U/mg pro,P<0.05]、降低高盐正常血压组左心室TNF-α[替米沙坦组(45.56±6.97)比高盐正常血压组(56.67±9.67)ng/g,均P<0.05]和高盐高血压组NF-κB[替米沙坦组(62.79±9.00)比高盐高血压组(87.77±10.30),P<0.05]表达水平。结论长期高盐饮食可导致Wistar大鼠心肌重构;氧化应激和炎症反应可能参与高盐诱导心肌重构的机制;替米沙坦可能部分通过抑制氧化应激、炎症反应,从而减轻高盐诱导的心肌重构。
Objective To observe the effect of high-salt diet on myocardial remodeling in Wistar rats and to explore the possible mechanism of telmisartan in reversing left ventricular remodeling. Methods Ninety-nine Wistar rats were randomly divided into high salt stress group (n = 12, NaCl: 2.015g / (d · d)] and high salt stress group [n = 12, NaCl: 2.015g / (Only · d)], while the control group [n = 13, NaCl about 0.094g / (only · d)] and the telmisartan group [n = 12 and NaCl about 1.966g / . The morphology and structure of myocardium were observed by HE and Masson staining. The activities of superoxide dismutase (SOD) and malondialdehyde (MDA) in the blood and left ventricle were measured by biochemical enzymatic method. The concentration of serum high sensitive C-reactive protein (hsCRP) was measured by enzyme linked immunosorbent assay (ELISA) (TNF-α) and Western blot were used to detect the expression of nuclear factor kappa B (NF-κB) p65 in myocardium. Results Compared with the control group, the levels of left ventricular mass index (LVMI), myocardial cell diameter (CMD), intermyocardial fibrosis area (MIFI), hsCRP, TNF-α concentration in left ventricle and NF-κB p65 protein expression (P <0.05). However, the activity of SOD in left ventricle was decreased. The remodeling of myocardium (LVMI, CMD and MIFI) was negatively correlated with the activity of SOD in left ventricle (r = -0.448 and -0.625, 0.492, all P <0.05], and positively correlated with the expression of NF-κB protein [r = 0.556,0.693,0.803, all P <0.05]; Telmisartan can improve the salt induced left ventricular remodeling, The SOD activity in the ventricles was significantly higher in the telmisartan group (72.20 ± 12.17 vs 58.34 ± 5.78, and in the high salt group (54.59 ± 6.65) U / mg pro, P <0.05] In the blood pressure group, TNF-α level in the left ventricle was significantly higher in the telmisartan group (45.56 ± 6.97 vs 56.67 ± 9.67 ng / g, P <0.05, respectively) and in the hypertensive group Saxan group (62.79 ± 9.00) than the high salt group (87.77 ± 10.30), P <0.05]. Conclusion Long-term high-salt diet can induce myocardial remodeling in Wistar rats. Oxidative stress and inflammatory response may be involved in the mechanism of high salt-induced myocardial remodeling. Telmisartan may reduce oxidative stress and inflammatory response, Induced myocardial remodeling.