發(fā)布時間：2018-07-31 19:31

【摘要】：目的:探討替米沙坦對心肌梗死后心力衰竭(心衰)大鼠左心室非梗死區(qū)激活素A及其受體表達的影響,闡明替米沙坦改善心肌膠原沉積的可能機制。方法:27只Wister大鼠分為假手術組(7只)、模型組(10只)和替米沙坦組(10只)。模型組和替米沙坦組大鼠結扎左冠狀動脈前降支,假手術組大鼠左冠狀動脈前降支僅穿線不結扎。建模后飼養(yǎng)5周,每組存活6只大鼠。假手術組大鼠給予0.5%CMC(10mL·kg~(-1)),模型組大鼠給予0.5%CMC(10mL·kg~(-1)),替米沙坦組大鼠給予替米沙坦(30mg·kg~(-1));連續(xù)灌胃給藥4周后測定大鼠全心肥厚指數及左心室肥厚指數,RT-PCR法測定大鼠左心室非梗死區(qū)心肌組織中激活素A、激活素Ⅱ型A受體(ActRⅡA)、Ⅱ型B受體(ActRⅡB)、Ⅰ型膠原蛋白(ColⅠ)和Ⅲ型膠原蛋白(ColⅢ)mRNA表達水平以及ColⅠ/ColⅢ比值;免疫組織化學染色觀察大鼠左心室非梗死區(qū)心肌組織中激活素A蛋白的表達強度。結果:與假手術組比較,模型組大鼠全心肥厚指數和左心室肥厚指數明顯升高(P0.01),激活素A、ActRⅡA、ActRⅡB、ColⅠ和ColⅢmRNA表達水平以及ColⅠ/ColⅢ比值升高(P0.01)。免疫組織化學染色,假手術組大鼠非梗死區(qū)心肌組織中激活素A蛋白呈低水平表達,模型組大鼠非梗死區(qū)心肌組織中激活素A蛋白呈高水平表達。結論:替米沙坦可能通過下調激活素A及其受體的表達水平改善心衰過程中心肌膠原沉積。
[Abstract]:Aim: to investigate the effect of telmisartan on the expression of activin A and its receptor in left ventricular non-infarct area of rats with heart failure after myocardial infarction, and to elucidate the possible mechanism of telmisartan in improving myocardial collagen deposition. Methods 27 Wister rats were divided into sham-operated group (n = 7), model group (n = 10) and telmisartan group (n = 10). The left anterior descending coronary artery was ligated in the model group and telmisartan group, while the left anterior descending branch was not ligated in the sham operation group. After 5 weeks of modeling, 6 rats in each group survived. 0.5%CMC (10mL kg ~ (-1), model group rats were given 0.5%CMC (10mL kg ~ (-1), telmisartan group) rats were given 30mg kg ~ (-1); for 4 weeks, total cardiac hypertrophy index (THR) and left ventricular hypertrophy index (LVH) were measured by RT-PCR. The mRNA expression levels of activin A, ActR 鈪，

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