LLLI对心肌梗死大鼠微RNA-21表达及心室重构的影响

Firoj Mk, Fa Xe, Yusuf Hb
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引用次数: 1

摘要

目的:探讨低水平激光照射(LLLI)对大鼠心肌梗死模型中微RNA-21表达及心室重构的影响。方法:将110只成年雌性SD大鼠随机分为假手术组(30只)、对照组(40只)和治疗组(40只)。对照组和治疗组结扎左前降支制备心肌梗死模型,假手术组在心肌梗死模型同一部位简单穿线。治疗组梗死区心肌梗死3周后,采用(635 nm, 6mW, 125s, 0.96 J/cm2)处理LLLI。在LLLI处理后1 h、24 h、48 h、72 h和7 d,采用qRT-PCR检测miR-21在梗死心肌组织中的表达。心肌梗死4周后,取心脏进行组织学分析。结果:治疗组MiR-21表达低于假手术组和对照组(P<0.05)。治疗组LLLI前后lvvef(%)、LVFS (%);(39.37±1.35∶47.62±2.75,P<0.05;(19.23±3.12)vs(24.15±2.53),P<0.05)。治疗组胶原纤维含量(28.79±2.06%)显著低于对照组(69.22±3.64%),差异有统计学意义(P<0.05)。结论:LLLI治疗心肌梗死可显著下调梗死区组织miR-21的表达,增加左心室功能,降低胶原纤维含量,提示LLLI对延缓心肌纤维化、减轻心肌梗死后病理性心室重构(VR)有有益作用。
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Effect of LLLI on Expression of Micro RNA-21 and Ventricular Remodeling inRats after AMI
Objective: To assess the effects of low-level laser irradiation (LLLI) on the expression of micro RNA-21 and ventricular remodelling in the model of rat myocardial infarction. Methods: 110 adult-female SD rats were randomly divided into sham operation (30), control (40), and treatment (40) groups. MI model was prepared by ligation of left anterior descending artery in the control and treatment groups while simply threading at the same site of MI model in sham group. LLLI treated using (635 nm, 6mW, 125s, 0.96 J/cm2) after three weeks of MI at infarct region in the treatment group. At 1 h, 24 h, 48 h, 72 h and 7 d after LLLI treatment, the expression of miR-21 at the infracted myocardial tissue were detected using qRT-PCR. At the end of 4 weeks after MI, hearts were harvested for histological analysis. Results: MiR-21 expression in the treatment group was lower than both sham group as well as the control group (P<0.05). LVEF (%) and LVFS (%) in the treatment group before and after LLLI; (39.37 ± 1.35 vs. 47.62 ± 2.75, P<0.05; (19.23 ± 3.12) vs (24.15± 2.53), P<0.05). Collagen fiber content in treatment group were significantly lower than control group (28.79 ± 2.06%) vs (69.22 ± 3.64%), (P<0.05). Conclusion: LLLI treatment of myocardial infarction can significantly down regulate the expression of tissue miR-21 in the infarct region, increase left ventricular function and decrease collagen fiber content suggesting the beneficial effect of LLLI on delaying myocardial fibrosis, reduce the pathological ventricular remodelling (VR) after MI.
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