肾去交感神经术对心力衰竭大鼠心功能及转化生长因子β1的影响

Effect of Renal Sympathetic Denervation on Cardic Function and the Expression of TGF-β1 in Rats with Heart Failure

目的探讨肾去交感神经术(renal sympathetic denervation,RDN)对心力衰竭大鼠心功能和心肌转化生长因子β1(transforming growth factor-β1,TGF-β1)表达水平的影响。方法成年雄性Wistar大鼠随机分为正常组对照组、单纯假手术组、肾去交感神经组(RDN组)、心力衰竭组4组。预处理后用异丙肾上腺素皮下注射法制作大鼠心力衰竭模型。心脏彩超评价大鼠心肌组织结构和功能的变化。Masson染色测算大鼠心肌胶原容积分数(collagen volume fraction,CVF),评价大鼠心肌纤维化程度。RT-PC法检测大鼠心肌TGF-β1mRNA的相对表达水平。免疫组化法测心肌组织TGF-β1蛋白的相对表达。结果RDN组大鼠左心室射血分数、左心室短轴缩短率高于心力衰竭组,而左心室舒张末期容积(ml)更低(射血分数:72.66%±7.95%vs 64.21%±6.23%,P<0.05;短轴缩短率:37.05%±5.30%vs 31.38%±1.65%,P<0.05;舒张末期容积:0.765±0.003 vs 0.912±0.002ml,P<0.05)。RDN组胶原容积分数低于心力衰竭组(13.96%±8.41%vs 59.69%±24.31%,P<0.05),TGF-β1mRNA的相对表达低于心力衰竭组(0.478±0.012 vs 0.896±0.025,P<0.05),TGF-β1蛋白表达平均吸光度值低于心力衰竭组(5.02±0.5 vs 6.99±0.39,P<0.05)。结论肾去交感神经术能抑制心力衰竭大鼠心肌纤维化并改善心功能,可能与抑制心肌组织TGF-β1的表达途径有关。

Objective To observe the effects of renal sympathetic denervation（RSD） on TGF - β1in heart failure rats. Methods Rats were randomly divided into control group, sham operation, RDN group and heart failure group. Intorduce heart failure rats model with isoprenaline. To evaluate the changes of cardiac structure and function of rat heart with ultrasound. Masson staining to measure the CVF. RT - PC method for the detection of myocardial TGF - β1 mRNA expression levels. Immunohistochemical staining was used to detect the relative expression of myocardial TGF - β1. Results In RDN group, left ventricular ejection fraction of rats, left ventricular fractional shorteningrate was higher than those of the heart failure group, and the left ventricular end diastolic volume （mL） was lower （left ventricular ejection fraction： 72.66 % ± 7.95 % vs 64.21% ± 6.23 % , P 〈 0.05 ;shortening rate： 37.05 % ± 5.30% vs 31.38 % ±1.65 % , P 〈 0.05; left ventricular end diastolic volume： 0. 765 ± 0. 003 vs 0. 912 ±0. 002ml,P 〈 0.05 ）. In RDN group, collagen volume fraction was lower than that of heart failure group （ 13.96%± 8.41% vs 59.69% ± 24.31% , P 〈 0.05 ）, and the relative expression of TGF - β1 mRNA was lower than hat of heart failure group （0. 478 ± 0. 012 vs 0. 896 ±0. 025 ,P 〈 0.05 ） , and the expression of TGF - β1 Average luminosity value was lower than the failure group （5.02 ± 0. 5 vs 6.99 ± 0.39,P 〈 0. 05）. Conclusion Renal sympathetic denervatiun can inhibit myocardial fibrosis in rats with chronic heart failureand improve heart function, which may be achieved by inhibiting the ex- pression of myocardial TGF - β1.