延冰通心片对大鼠心肌梗死的保护作用及作用机制研究

Study on Protective Effects and Mechanism of Yanbing Tongxin Tablets on Rats with Myocardial Infarction

目的观察延冰通心片对大鼠心肌梗死模型的影响并探讨其作用机制。方法通过异丙肾上腺素诱导建立心肌梗死模型。将50只Wistar雄性大鼠随机分成空白对照组、心肌梗死模型组、延冰通心片低剂量组、延冰通心片高剂量组及卡托普利组。空白对照组及心肌梗死模型组灌胃蒸馏水,延冰通心片低剂量组灌胃延冰通心片溶液,剂量为30 mg/kg/d,延冰通心片高剂量组灌胃延冰通心片溶液,剂量为60 mg/kg/d,卡托普利组灌胃卡托普利溶液,剂量为50 mg/kg/d,所有组大鼠灌胃给药体积均为20 mL/kg/d。给药4周后测定各组大鼠体内血浆内皮素(ET)、心钠素(AN P)、醛固酮(ALD)、血管紧张素(AngⅡ)含量及心肌AngⅡ含量。测定各组大鼠血清中乳酸脱氢酶(LDH)、天门冬氨酸氨基转移酶(AST)、肌酸激酶(CK)及肌酸激酶同工酶(CKMB)的活性。结果延冰通心片能明显降低心肌梗死大鼠血浆ET、ANP、ALD、AngⅡ含量及心肌AngⅡ含量,还能够降低乳酸脱氢酶(LDH)、天门冬氨酸氨基转移酶(AST)、肌酸激酶(CK)及肌酸激酶同工酶(CKMB)的活性。结论延冰通心片对异丙肾上腺素诱导的大鼠心肌梗死具有保护作用,可能与其抑制肾素血管紧张素醛固酮系统,降低缩血管物质含量进而保护心肌细胞有关。

Objective To observe the effect of Yanbing Tongxin tablets on myocardial infarction model in rats, and to explore its mechanism. Methods With large dosage injection of isoproterenol to establish rat myocardial fibrosis model, the wistar rats were divided into 5 groups, including sham operation group, Myocardial infarction model group, Yanbing Tongxin tablets low group, Yanbing Tongxin tablets high group and Captopril group. The rats in sham operation group and remodeling model group were fed with distilled water. The Yanbing Tongxin tablets group was treated Yanbing Tongxin tablets （with 30mg·kg^-1·d^-1 or 60mg·kg^-1·d^-1） . The Captopril group was treated Captopril （with 50mg·kg^-1·d^-1, i.g） . After 4 weeks, the content of endothelin （ET） , antrial natriuretic peptide （ANP） , aldosterone （ALD） , angiotensin Ⅱ （Ang Ⅱ ） in plasma were determined. The CK, CKMB, AST and LDH activities in serum were also determined. Results After treatmentby Yanbing Tongxin tablets, the content of ET, ANP, ALD, Ang Ⅱ in plasma were declined, the Ang Ⅱ content in myocardial was also declined in Yanbing Tongxin tablets low group, Yanbing Tongxin tablets high group. In addition, the CK, CKMB, AST and LDH activities were significantly decreased in Yanbing Tongxin tablets low group, Yanbing Tongxin tablets high group. Conclusion Yanbing Tongxin tablets has protective effect on rats＇ isoproterenol-induced myocardial infarction by inhibiting renin angiotensin aldosterone system, reducing vasoconstrictor content to protect cardiomyocytes.