肖立中,黄志,马绍椿,曾兆俞,罗碧容,林晓云,徐新.葛根素对急性心肌梗死患者梗死面积的影响及其机制探讨[J].,2004,(9):790-792 |
葛根素对急性心肌梗死患者梗死面积的影响及其机制探讨 |
Study on the Effect and Mechanism of Puerarin on the Size of Infarction in Patients with Acute Myocardial Infarction |
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DOI: |
中文关键词: 葛根素 急性心肌梗死 自由脂肪酸 C-反应蛋白 基质金属蛋白酶-9 |
英文关键词:puerarin acute myocardial infarction free fatty acids C-reactive protein matrix metalloproteinases-9 |
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中文摘要: |
目的探讨葛根素对急性心肌梗死患者梗死面积及脂肪酸代谢、炎症反应及斑块稳定性的影响。方法 6 1例急性心肌梗死患者随机分为对照组 (30例 )和葛根素组 (31例 ) ,两组均予常规治疗 ,葛根素组加用葛根素 5 0 0mg/d ,疗程 2周。测定治疗前后血浆游离脂肪酸、基质金属蛋白酶 9(matrixmetalloproteinases 9,MMP 9)、C 反应蛋白水平及用IdekerQRS记分法测定梗死面积。结果治疗前血浆自由脂肪酸、MMP 9、C 反应蛋白与梗死面积呈正相关 (r =0 4 3、0 4 2、0 39,P <0 0 1) ;与治疗前比较 ,葛根素组自由脂肪酸、MMP 9及C 反应蛋白分别降低 30 %、4 1%、2 3% ,梗死面积明显缩小 (P <0 0 1) ,对照组无明显变化 (P >0 0 5 )。结论葛根素治疗可明显缩小急性心肌梗死面积 ,可能与降低血浆自由脂肪酸、抑制炎症及稳定动脉粥样硬化斑块有关 |
英文摘要: |
Objective To observe the effect of puerarin on infarction size, fatty acids metabolism, inflammatory response and atherosclerotic plaque stability in patients with acute myocardial infarction (AMI). Methods Sixty one patients with AMI were randomly divided into two groups, the control group (n=30) and the treated group (n=31). All were treated with conventional treatment, but to the treated group, puerarin injection was given additionally by injecting 500mg per day for 2 weeks. Before and after treatment, blood levels of free fatty acids (FFA), matrix metalloproteinases 9 (MMP 9) and C reactive protein (CRP) were assayed, and the size of infarction was determined by Ideker QRS scoring method. Results Before treatment, the size of infarction was positively correlated to the levels of FFA, MMP 9 and CRP (r = 0.43, 0.42 and 0.39, respectively, all P< 0 01). As compared with those before treatment, after treatment, the three parameters lowered by 30%, 41% and 23%, respectively and the size of infarction significantly reduced in the treated group (P<0 01), while in the control group, no significant change was found (P>0 05). Conclusion Puerarin treatment could significantly reduce the size of infarction in patients with AMI, the mechanism is possibly related with its effects in lowering plasma levels of FFA, inhibiting inflammation and stabilizing atherosclerotic plaque |
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