EGCG抑制心肌肥厚胶原生成和细胞增殖

EGCG inhibition against collagen accumulation and cell proliferation in cardiac hypertrophy

目的研究表没食子儿茶素没食子酸酯(EGCG)的抗心肌肥厚作用以及对心肌肥厚胶原生成和细胞增殖的影响。方法异丙肾上腺素(Iso)致小鼠心肌肥厚,测定心脏重量指数和血清乳酸脱氢酶(LDH)、肌酸磷酸激酶(CK)活力。腹主动脉缩窄致大鼠心肌肥厚,测定心脏重量指数和心肌羟脯氨酸(Hp)含量,HE和VG染色观察心肌组织形态改变,增殖性核抗原(PCNA)免疫组化检测细胞增殖。结果EGCG50、100、200mg.kg-1剂量依赖的降低Iso致小鼠心肌肥厚的心脏重量指数及血清LDH、CK的漏出量。EGCG25、50、100mg.kg-1剂量依赖的降低腹主动脉缩窄致大鼠心肌肥厚的心脏重量指数和心肌Hp含量,明显改善心肌组织胶原增生和纤维化,EGCG50、100mg.kg-1明显降低细胞PCNA免疫组化阳性率。结论EGCG对大鼠和小鼠心肌肥厚模型有明显的抑制作用,该作用可能与改善肥厚心肌组织胶原增生和细胞增殖有关。

Aim To study the effects of EGCG on cardiac hypertrophy in mice and rats and to investigate the effects of EGCG on collagen accumulation and cell proliferation in cardiac hypertrophy. Methods Cardiac hypertrophy in mice was induced by continued administration of isoprenaline （Iso）. Heart we serum lactate dehydrogenase （LDH） ight indexes, and creatine phosphokinase （CK） activity were investigated. Cardiac hypertrophy in rats was established by abdominal aortic constriction. Heart weight indexes and hydroxyproline （Hp） in heart tissue were detected. HE and VG stain were used to detect the cardiac morphological changes. Proliferating cell nuclear antigen （PCNA） immonochemistry was used to detect cell proliferation in heart tissue. Results In cardiac hypertro-phy induced by continued administration of Iso in mice, EGCG 50, 100, 200 mg·kg^-1 dose-dependently reduced heart indexes, serum LDH and CK activity. In cardiac hypertrophy induced by abdominal aortic constriction in rats, EGCG 25, 50, 100 mg·kg^-1 dose-dependently reduced heart indexes and Hp content in heart tissue. In HE and VG stain, EGCG inhibited collagen accumulation and fibrosis markedly. EGCG 50, 100 mg·kg^-1 reduced PCNA positive cells in heart tissue. Conclusion EGCG significantly inhibits cardiac hypertrophy in mice and rats, which may be related to the reduction in proliferation of cardiac collagen accumulation and tissue.