摘要
目的探讨G-CSF的作用机制,为临床药物治疗提供依据。方法健康SD大鼠50只随机分为4组:A组(n=5)为正常组,B组(n=5)为药物动员组,C组(n=20)为急性心肌梗死(AMI)组,D组(n=20)为药物动员+AMI组。C、D两组于术后1d、5d、9d、14d分批处死,收集标本检测。G―CSF给药方法:皮下注射10μg/kg.d,共5d。采用液氮损伤造成大鼠AMI模型。酶联免疫吸附法(ELISA)测定血清血管内皮生长因子(VEGF)浓度,免疫组化测定心肌中血管内皮生长因子(VEGF)的含量和毛细血管密度。结果(1)B组、术后1dC组和术后1dD组血清中VEGF浓度均显著高于A组(P均小于0.05)。(2)术后1d、5d、9d、14dD组血清中VEGF浓度均明显高于C组(P<0.05)。(3)术后1d、5d、9d、14dD组心肌梗死区VEGF含量均明显高于C组(P<0.05)。(4)术后1d、5d、9d、14dD组心肌梗死区毛细血管密度均明显高于C组(P<0.05)。结论G―CSF能促进大鼠急性心肌梗死区毛细血管增生,其部分机制可能为通过增强VEGF分泌实现。
Objective To research the angiogenesic effects and mechanism of G-CSF on experimental acute myocardial infarction rats. Methods 50 rats were randomly divided into A,B,C and D groups. Group A （n=5）： control ; Group B （n=5）： G-CSF; Group C（n=20）： AMI; Group D （n=20）： G-CSF＋AMI. Animals of group C and D were sacrificed in batches on 1, 5, 9 and 14 days postoperatively . Blood samples and myocardial specimeus were obtained for experimental study. G-CSF was given consecutively 5 days by hypodermic injection （10μg/kg.d）. A freeze-thaw injury model was used to induce AMI. Vascular endothelial growth factor（VEGF） in bood was measured by ELISA. With the use of immuno-histochemical staining, VEGF and neovessel density in myocardial infarction area were measured Results Compared with control , blood concentration of VEGF in group B, C and D were significantly increased （all with P〈0.05）. At 1, 5, 9 and 14 days after operation, the increase of blood VEGF concentration in group D were higher than that in group C. Also,the same appearance were observed on VEGF expression and angiogenesis in myocardial infarction area between group D and C. Conclusion Hypodermic injection of G-CSF may cause an enhanced angiogenesis of acute myocardical infarction tissue in experimental rats. The angiogenesic effects of G-CSF are obtained partly by upregulation of local myocardial tiusse and blood VEGF expression .
出处
《江西医药》
CAS
2006年第8期550-552,共3页
Jiangxi Medical Journal
基金
江西省卫生厅课题
