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辛伐他汀对压力超负荷大鼠APN、IL-6及心肌肥厚影响 被引量:6

EFFECT OF SIMVASTATIN ON SERUM ADIPONECTIN,INTERLEUKIN-6 AND CARDIAC HYPERTROPHY INDUCED BY PRESSURE OVERLOAD IN RATS
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摘要 目的观察辛伐他汀对压力超负荷大鼠血清脂联素(APN)、白细胞介素-6(IL-6)水平以及心肌肥厚的影响,探讨该类药物影响心肌肥厚可能的作用机制。方法实验动物随机分对照组、心肌肥厚组、治疗组,每组10只。应用经典的腹主动脉结扎方法,制备压力超负荷大鼠模型。治疗组大鼠给予辛伐他汀5mg/kg每日清晨灌胃,连续6周。心肌肥厚组和对照组同时以同等剂量的9g/L的氯化钠溶液每日清晨灌胃,直至术后6周。采用鼠尾测压法测定大鼠血压的变化;酶联免疫吸附试验法检测大鼠血清APN、IL-6浓度。实时定量PCR检测心肌组织中IL-6、脂联素受体1(AdipoR1)的mRNA表达。称量法计算各组大鼠心脏质量及心脏质量/体质量比值,并观察心肌的病理学改变。结果心肌肥厚组大鼠血清APN水平、IL-6水平、心脏质量、心脏质量/体质量比值、左心室壁平均厚度、心肌细胞平均直径,以及心肌IL-6、AdipoR1mRNA表达与对照组相比差异有显著性(q=3.41~31.83,P<0.01)。治疗组大鼠与心肌肥厚组相比血清APN水平、IL-6水平、心脏质量、心脏质量/体质量比值、左心室壁平均厚度、心肌细胞平均直径以及心肌IL-6、AdipoR1mRNA表达差异有显著性(F=3.57~329.93,q=3.11~31.08,P<0.01)。结论辛伐他汀可能通过增加血清APN的浓度以及心肌细胞因子的表达来抑制压力负荷增加引起的大鼠心肌肥厚。 Objective To study the effect of simvastatin on serum adiponectin (APN), interleukin-6 (IL-6) and cardiac hypertrophy in pressure-overload rats. Methods A rat model was established by classical technique through ligature of abdominal aorta. Thirty Wistar rats were evenly divided into normal control, cardiac hypertrophic, and treated groups. Simvastatin [5 mg/(kg · d)] was given intragastrically every morning; the rats in normal control and cardiac hypertrophic were given normal saline (9 g/L), medication was given once every morning for six weeks in all three groups. Systolic blood pressure was measured using the tail cuff method. Serum adiponeetin and IL 6 were detected by ELISA, mRNA expression of IL 6 and serum adiponectin receptor were analyzed by real-time PCR, the heart weight, the ratio of heart weight to body weight calculated. The pathological changes of the hearts were measured. Results The differences between control and cardiac hypertrophy groups were significant in terms of APN and IL-6, mRNA expression of AdipoR1 and IL-6, the cardiac weight, ratio between heart weight and body weight, the average thickness of left ventricle wall, and the average diameter (F=3.57- 329.93, q= 3.41- 31.83, P〈0.01). The differences between cardiac hypertrophy group and treated groups were significant in terms of serum APN and IL-6, mRNA expression of AdipoR1 and IL-6, the cardiac weight, ratio between heart weight and body weight, the average thickness of left ventricle wall, and the average diameter (q=3.11--31.08,P〈0.01). Conclusion Simvastatin is likely to suppress pressure-over load myocardial hypertrophy in rats through increasing the concentration of serum adiponectin and the expression of cadiocite cells.
出处 《青岛大学医学院学报》 CAS 2009年第1期60-62,64,共4页 Acta Academiae Medicinae Qingdao Universitatis
关键词 心室重构 辛伐他汀 脂联素 白细胞介素6 大鼠 WISTAR Ventricular remodeling Simvastatin Adiponectin Interleukin-6 Rats, Wistar
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参考文献8

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