【摘要】 目的研究复方缬芎滴丸(VLC)对心肌细胞缺氧再给氧损伤的保护作用,并探讨其作用机制。方法采用血清药理学的研究方法,对大鼠进行灌胃给予VLC,剂量分别为32 mg.kg-11、6 mg.kg-1,空白组给予等体积生理盐水;制备含药血清,将含药血清加入培养5 d的乳鼠心肌细胞中,阳性组直接加入川芎嗪;厌氧培养24 h后,更换培养基(含有受试药),再给氧4 h,阴性对照组一直置于常规下培养;最后,检测培养基上清中的乳酸脱氢酶(LDH)及细胞中丙二醛(MDA)含量;消化受试乳鼠心肌细胞制成细胞悬液,进行碘化丙啶染色,用流式细胞仪检测心肌细胞凋亡百分率。结果与正常组相比,缺氧再给氧损伤组LDH、MDA含量均增高,说明细胞在缺氧再给氧后脂质过氧化增强,心肌细胞出现明显的损伤。与模型组相比,VLC各含药血清组LDH、MDA值均明显降低,表明VLC有抗心肌细胞脂质过氧化的作用。流式细胞仪检测结果显示VLC含药血清组心肌细胞凋亡率分别降低38%、69%(P<0.01),表明VLC可降低缺氧再给氧后心肌细胞凋亡百分率。结论VLC对急性心肌缺血有明显的保护作用,其作用机制可能是VLC能够降低心肌缺血时氧自由基的产生,并有抗心肌细胞凋亡的作用。更多还原

【Abstract】 Objective To study the protective effect of VLC on myocardial cells injured by hypoxia-reoxygenation and its mechanism.Methods Serum pharmacology method was used in this study.After 5 days treatment with VLC 32 mg/kg,16 mg/kg in rats,the serums were separated and added into culture medium.Then,the myocardial cells of neonatal rats were cultured under hypoxia condition for 24 h,followed by reoxygenation for 4 h.Finally,the LDH and MDA were examined.To get the apoptosis rate,the FCM was used.(Results Compared) with normal group,the content of LDH,MDA in hypoxia-reoxygenation group increased,VLC had anti-apoptosis effect in myocardial cells by decreasing the production of ROS.Conclusion VLC has protective effect on myocardial cells,and its anti-apoptosis effect in myocardial cells is to decrease the production of ROS.更多还原