目的:探讨G蛋白抑制肽GCIP-27对去甲肾上腺素诱导的小鼠心肌肥大的作用。方法:50只小鼠随机分为对照组、模型组和GCIP-27组,分别给予生理盐水、去甲肾上腺素和GCIP-27低、中、高剂量(10、30、100μg·kg^-1)连续15d。之后称量小鼠体质量、心脏重、左心室重,计算心脏指数和左心室指数。采用免疫组化法测定心肌组织的原癌基因c-Fos和细胞外信号调节激酶P—ERK1/2表达。结果:与对照组比较,模型组可明显诱导小鼠产生心肌肥大。与模型组比较,GCIP-27各剂量组能明显降低心脏指数和左心室指数,减少心肌组织中c-Fos和P—ERK1/2的表达量(P〈0.05或P〈0.01)。结论:GCIP-27可抑制小鼠发生心肌肥大,其机制可能与抑制c-Fos和p-ERK1/2表达有关。
OBJECTIVE: To explore the effect of G protein inhibitory peptide GCIP-27 on the myocardial hypertrophy induced by noradrenaline (NA) in mice. METHODS: Fifty mice were randomly divided into five groups: control group, NA group and GCIP-27 (10, 30, 100 μg·kg^-1) groups. Each group was administrated with normal saline, NA and GCIP-27 10, 30, or 100μg·kg^-1 respectively. After 15 days' treatment, all the mice were killed to weigh their body, heart and left ventricle and the cardiac hypertrophy indexes including heart index and left ventricular index were measured. The expression of c-Fos and p-ERK1/2 in myocardium were determined using immtmohistochemistry technique. RESULTS: Compared with the control group, NA could obviously induce rats to have cardiac hypertrophy. Compared with the NA group, treatment with GCIP-27 (10, 30 or 100 μg·kg^-1) decreased the heart index, left ventricular index significantly. Moreover, GCIP-27 decreased the expression of e-Fos and p-ERK1/2 in myocardium markedly (P〈0.05 or P〈0.01). CONCLUSION: GCIP-27 can attenuate cardiac hypertrophy which may be related to the restraint of the expression of c-Fos and p-ERK1/2 in myocardium.