【作者】 郭洁文； 李丽明； 邓志军； 符永恒； 杨敏； 单绮霞； 潘竞锵； 刘若轩；

【Author】 GUO Jie-wen1,LI LI-ming1,DENG Zhijun1,FU Yong-hen2,YANG Min2, SHAN Yi-xia3,PAN Jing-qiang1,LIU Ruo-Xuan1(1.Guangzhou Hospital of Traditional Chinese Medicine, Guangzhou 510130,China;2. Research Center of Medical Science, Guangdong Provincial People’s Hospital, Guangzhou 510080, China ; 3.The Peple’s Hospital of Zhengcheng ,Guangzhou 511300, China)

【机构】 广州市中医医院； 广东省人民医院医学研究中心； 广东省心血管病研究所； 中山大学附属博济医院药剂科；

【摘要】 目的研究三七总皂苷(PNS)对急性心肌梗塞后左室重构血管紧张素转换酶2(ACE2)与大鼠肿瘤坏死因子α(TNF-α)表达的影响。方法采用结扎大鼠左冠状动脉前降支的方法建立AMI模型,术后24h后随机分为对照组和实验组,连续4周分别灌胃给予生理盐水、福辛普利和PNS低、中、高剂量,观察PNS对病鼠血清丙二醛(MDA)、一氧化氮(NO)、谷胱甘肽过氧化物酶(GSH-Px)、ACE2与TNF-α含量的影响。结果PNS与福辛普利均能显著降低MDA,提高GSH-Px活性(P<0.01～0.05),高剂量PNS还可明显降低NO含量(P<0.05),PNS低、中、高剂量组均能刺激ACE2的释放,并减少TNF-α的表达(P<0.05)。结论PNS可通过刺激病鼠ACE2的释放,抑制脂质过氧化反应及TNF-α表达,减轻心肌细胞损伤保护心肌,改善心室重构。更多还原

【Abstract】 OBJECTIVE Research on effects of panax notoginsenoside (PNS) on angiotensin-converting enzymes(ACE2)and tumor necrosis factor-α (TNF-α) in rats with post-myocardial infarction ventricular remodeling. METHODS Models of acute myocardial infarction (AMI) were produced by ligation of left anterior descending coronary artery, building rat model of AMI, after 24 hours of postoperative in rats.The rats were randomly divided into controlled and experimental groups,then respectively gavaged with NS,fosinopril and low,middle and high dosage of PNS for four consecutive weeks. To observe effects of PNS on malondialdehyde (MDA),nitric oxide(NO),glutathione peroxidase (GSH-PX), ACE2 and TNF-α in rats with post-myocardial infarction ventricular remodeling. RESULT Compared with the NS group, MDA is significantly lower,the activity of GSH-PX significantly enhanced(P <0.01～0.05), NO of the high-dose PNS group can be decreased(P<0.05), Compared with the NS group, ACE2 can be increased and TNF-α can be significantly decreased by PNS in low,middle and high dosage groups (P<0.05). CONCLUSION PNS can stimulus ACE2 to inhibit the expression TNF-α, enhance the antioxidance.PNS can reduce pathological injury of cardiac myocytes in myocardial ischemia and cardiac muscle ,which can improve ventricular remodeling更多还原