【摘要】 目的　目的研究当归抗心肌缺血 /再灌注损伤的分子生物学机制。方法　结扎 /开放左冠状动脉前降支结扎 40min/开放 12 0min建立心肌缺血 /再灌注模型。选用SD大鼠 40只 ,随机分成三组 :对照组 (A组 ,n =10只 ) ,丝线穿过冠状动脉前降支但不结扎 ;缺血 /再灌注组 (B组 ,n =15只 ) ,缺血 /再灌注前舌静脉注射生理盐水 0 8ml/ 10 0 g ,当归治疗组 (C组 ,n =15只 ) ,缺血再灌注前舌静脉注射 2 5 %当归注射液 0 8ml/ 10 0 g。采用免疫组化SP法测定蛋白激酶C(PKC)含量和同位素标记法测定PKC活性。结果　与B组比较 ,C组心肌梗死面积显著缩小 (P <0 0 1) ,A组及C组PKC灰度值显著性降低 (P <0 0 1) ,A组PKC的活性无显著性差异 (P >0 0 5 ) ,而C组PKC活性明显升高 (P <0 0 1)。与A组比较 ,C组PKC的灰度值无显著性差异 (P >0 0 5 ) ,PKC的活性明显升高(P <0 0 1)。C组的PKC多分布在细胞膜上 ,A组及B组的PKC多分布在细胞核和细胞浆内。结论　当归可促使PKC从细胞核转移到细胞膜 ,从而激活PKC抑制心肌缺血 /再灌注损伤。更多还原

【Abstract】 Objective To study the molecular biological mechanism of the protective effect of angelica on myocardium during ischemia reperfusion Methods The myocardial ischemia/reperfusion was induced with the 40 min cross clamp/120 min declamping of anterior decending coronary artery Forty SD rats were randomly divided into 3 groups: group A without myocardial ischemic reperfusion , group B with intravenous adminisrtration of normal saline 0 8ml/100g before ischemia reperfusion , and group C with intravenous adminisrtration of 25% angelica 0 8ml/100g before ischemia reperfusion The content of protein kinase C (PKC) in cardiac myocyte was measured with immunohistochemical method, and the PKC activity with the isotope lable method Results Compared with those in group B, the myocardial infarct size reduced significantly in group C (P<0 01), the grey value of PKC decreased markedly in group A or C(P<0 01),the PKC activity remained unsignificant change in group A (P>0 05) but increased obviously in group C (P<0 01) There was not significant difference in the grey value of PKC between group C and A (P>0 05) The PKC activity was significantly higher in group C than that in group A(P<0 01) PKC was located at cellular membrane in group C, but at cellular nucleus or in cellular plasm in groups A and B Conclusions Angelica can protect myocardium from ischemia reperfusion injury through activation of PKC by impelling PKC to transfer from cellular nucleus or cellular plasm to cellular membrane更多还原