蜕皮甾酮对大鼠急性心肌梗塞侧支循环形成及VEGF产生的影响

目的　研究蜕皮甾酮 (ecdysterone ,EDS)对大鼠急性心肌梗塞侧支循环形成的促进作用 ,以及上述过程实现的基本机制是否与蜕皮甾酮上调心肌细胞分泌产生血管内皮生长因子 (VEGF)有关。方法　①建立Wistar大鼠急性心肌梗塞模型 ,实验组给予蜕皮甾酮治疗 7d后进行血清心肌酶测定 ;免疫组化检测VEGF表达 ;Ⅷ因子相关抗原标记内皮细胞 ,检测毛细血管密度。②原代培养大鼠心肌细胞在常氧与缺氧状态下 ,实验组分别给于蜕皮甾酮治疗 ,2 4h后进行免疫组化检测心肌细胞中血管内皮生长因子表达 ,经计算机扫描 ,图像分析定量。结果　与对照组相比 ,蜕皮甾酮治疗组大鼠血清肌酸激酶同工酶 (CK MB)明显降低〔(5 4 10 0±3 15 4)vs (73 5 5 7± 3 2 80 )U·L-1,P <0 0 1〕 ;VEGF表达增强〔(17 76 2± 1 42 0 )vs (2 0 90 5± 0 976 ) ,P <0 0 1〕 ;毛细血管密度增加〔(1 12 7%± 0 147% )vs (0 793 %±0 0 76 % ) ,P <0 0 1〕。在常氧与缺氧状态下 ,蜕皮甾酮治疗组心肌细胞VEGF表达高于对照组〔(2 5 0 0 0± 0 5 44 )、(2 1 2 86± 1 0 96 )vs (31 381± 0 912 )、(2 3 5 71± 0 95 7) ,P <0 0 1〕。结论　蜕皮甾酮通过刺激心肌分泌VEGF ,促进大鼠缺血区侧支循环建立 ,增加毛细血管密度 ,发挥心肌保护作用

Effects of ecdysterone on collateral formation and expression of VEGF in rat AMI

AIM\ To determine if ecdysterone(EDS) could enhance collateral formation in rat acute myocardial infarction(AMI),whether the basic mechanism is that EDS influences expression of vascular endothelial growth factor(VEGF) in myocardium METHODS\ ① Experimental groups received EDS 40 mg·d -1 in each rat AMI After 7 d,myocardial enzymes in serum were detected;VEGF and microvascular density were also detected with immunohistochemical technique ②Experimental groups of primary culture of rat cardiac myocytes received EDS 100 mg·L -1 in normal and hypoxia condition After 24 h,VEGF was detected in the same way ③Computer scanned and quantitated RESULTS EDS reduced the concentration of myocardial enzymes(CK MB) in serum 〔(54 100±3 154) U·L -1 vs (73 557±3 280) U·L -1 , P< 0 01〕; enhance the production of VEGF 〔(17 762±1 420) vs (20 905±0 976), P< 0 01〕 and the formation of collateral circulation and microvascular density〔(1 127%±0 147%) vs (0 793%±0 076%), P< 0 01〕 In addition, EDS could enhance expression of VEGF in rat cardiac myocytes in normal 〔(25 000±0 544) vs (31 381±0 912) , P< 0 01〕 and hypoxia condition 〔(21 286±1 096) vs (23 571±0 957), P< 0 01〕. CONCLUSION EDS may promote the establishment of cardiac collateral circulation and enhance microvascular density in infarction zone by upregulation of VEGF protein expression