摘要
为了探讨川芎嗪对心肌缺血 再灌注损伤 (MIRI)时心肌细胞线粒体功能及结构的影响。本实验选用日本大耳白兔 30只 ,随机分为正常对照组 (A组 )、心肌缺血 再灌注损伤组 (B组 )和心肌缺血 再灌注损伤 +川芎嗪治疗组(C组 )。复制MIRI模型 ,分别观察心肌线粒体呼吸功能、Ca2 + 浓度 ([Ca2 + ]m)、丙二醛浓度 (MDA)、超氧化物歧化酶活性 (SOD)及超微结构的改变和心肌组织三磷酸腺苷 (ATP)、二磷酸腺苷 (ADP)、一磷酸腺苷 (AMP)含量、总腺苷酸量 (TAN)、能荷 (EC)的变化。结果发现 ,C组与B组比较 ,线粒体呼吸控制率 (RCR)、Ⅲ态呼吸速率 (ST3)、SOD、面密度 (Sv)、比表面 (δ)明显升高 ,Ⅳ态呼吸速率 (ST4 )、[Ca2 + ]m 、MDA、体密度 (Vv)、横径 (Hd)显著降低 ,心肌组织ATP、ADP、TNA及EC均明显增高 ;且与A组比较 ,ST3、ST4 、SOD、Vv、Sv、δ、数密度 (Nv)、纵径 (Vd)及ADP、AMP、TNA无明显差异。可见 ,川芎嗪可通过降低氧自由基水平和减轻钙超载 ,而改善缺血 再灌注损伤心肌的线粒体功能及结构。
To study the effect of ligustrazini (LGT) on function and structure of mitochondria in myocardial cell during myocardial ischemia-reperfusion injury (MIRI). Using MIRI model in rabbits,animals were randomly divided into three groups (n=10 in each):control group(A),MIR group (B) and MIR+LGT group (C),the mitochondrial respiratory function、Ca 2+ concentration([Ca 2+] m) 、malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were determined.Meanwhile,the contents of ATP、ADP and AMP (TAN、E) in the myocardial tissue were measured respectively. Moreover,the ultrastructure changes in myocardial mitochondria were observed during MIRI. It was found that mitochondrial respiratory control rate (RCR)、state 3 (ST 3)、SOD、surface density (Sv) and specific surface (δ) in C group were higher than those of group B, state 4 (ST 4)、[Ca 2+] m、MDA、volume density (Vv)、horizental diameter (Hd) were lower than those of group B,ATP、ADP、TAN and EC levels of myocardial tissue were higher than those in group B;and there were not significant differences between group C and A about ST 3、ST 4、SOD、Vv、Sv、δ、Nv、Vd and ADP、AMP、TNA.It is suggested that LGT can improve function and structure of mitochondria in myocardial cell in the reperfusion injury after myocardial ischemia by decreasing oxygen free radical level and Ca 2+ overload in the mitochondria.
出处
《基础医学与临床》
CSCD
北大核心
2004年第3期295-298,共4页
Basic and Clinical Medicine
基金
浙江省跨世纪学术和技术带头人培养基金 (992 0 86 )
温州市"5 5 1人才工程"培养基金 (98113)
温州市科技局(S2 0 0 0A2 4 )
浙江省卫生厅优秀青年科研基金联合资助项目 (2 0 0 1QN0 13)