| 曹瑜梦,刘 洋,郭统帅,马云龙,吴 岳,方 媛.miR-506与PI3K/AKT通路在自发性高血压大鼠心脏重构中的作用[J].,2018,(19):3607-3611 |
| miR-506与PI3K/AKT通路在自发性高血压大鼠心脏重构中的作用 |
| The Effects of miR-506 and PI3K/AKT Pathway in Cardiac Remodeling of Spontaneous Hypertensive Rats |
| 投稿时间：2018-03-25 修订日期：2018-04-23 |
| DOI：10.13241/j.cnki.pmb.2018.19.002 |
| 中文关键词: 自发性高血压 miR-506 氧化应激 PI3K/AKT通路 |
| 英文关键词: Spontaneous hypertension miR-506 Oxidative stress PI3K/AKT pathway |
| 基金项目:国家自然科学基金项目（30900616） |
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| 中文摘要: |
| 摘要 目的：探讨miR-506和PI3K/AKT信号通路在自发性高血压大鼠心脏重构中的作用。方法：将12只雄性自发性高血压大鼠(Spontaneous Hypertension Rat, SHR)随机分为2组，每组6只。分别为SHR模型组和治疗组（卡托普利，30 mg?kg-1），6只健康WKY大鼠作为空白对照组。SHR模型组和空白对照组灌胃等体积生理盐水，连续给药8周，采用尾动脉测压法测定给药前后各组大鼠血压，采用qRT-PCR法检测各组大鼠心肌miR-506表达量，并检测大鼠心肌组织中SOD和GPx mRNA表达水平，免疫印迹检测大鼠心肌中p-PI3K和p-AKT的蛋白表达量。结果：SHR模型组血压为（184.79±3.35）mmHg，与空白对照组比较显著升高（P<0.05），治疗组血压为（133.57±1.43）mmHg，与SHR模型组相比均显著降低（P<0.05）。SHR模型组大鼠心肌中miR-506、SOD、GPx的RNA相对表达量分别为（0.36±0.05）、（0.27±0.04）和（0.32±0.02），与空白对照组比较显著降低（P<0.05），而p-PI3K、p-AKT蛋白水平显著降低（P<0.05），与SHR模型组比较，治疗组大鼠心肌中miR-506以及SOD、GPx 的RNA水平显著升高（P<0.05），p-PI3K、p-AKT蛋白水平显著升高（P<0.05）。结论：在卡托普利治疗高血压的过程中，miR-506可能通过抑制PI3K/AKT信号通路提高机体的抗氧化能力促进SHR心脏重塑。 |
| 英文摘要: |
| ABSTRACT Objective: To investigated the effects of miR-506 and PI3K/AKT Pathway in cardiac remodeling of spontaneous hy- pertensive rats. Methods: 12 male SHR rats were randomly divided into 2 groups (6 in each group) included SHR model group and treat- ment group (captopril, 30 mg?kg-1). 6 WKY rats were regard as blank control group. SHR model group and blank control group were giv- en equal volume of normal saline. The rats were treated for eight weeks. The blood pressure before and after the experiment was mea- sured by tail artery measurement. The expression of miR-506, SOD and GPx mRNA in myocardium of rats was detected by qRT-PCR and the expression of p-PI3K and p-AKT protein was detected by western blotting. Results: The blood pressure of the SHR model group (184.79±3.35 mmHg) was significantly higher than that of the blank control group(P<0.05). The blood pressure of the treatment group (133.57±1.43 mmHg) was significantly lower than that of the SHR model group(P<0.05). Compared with the blank control group, the RNA levels of miR-506 (0.36±0.05), SOD (0.27±0.04) and GPx (0.32±0.02) in the myocardium of the SHR model group were signifi- cantly decreased(P<0.05), and the levels of p-PI3K and p-AKT protein were significantly increased(P<0.05). Compared with the SHR model group, the levels of miR-506, SOD and GPx mRNA in the myocardium were significantly increased(P<0.05), and the levels of p-PI3K and p-AKT protein were significantly decreased in treatment groups (P<0.05). Conclusion: miR-506 may promote the progress of cardiac remodeling by improving the antioxidant capacity of the myocardium through inhibition of PI3K/AKT pathway. |
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