缩醛基毛冬青提取化合物R4对大鼠急性心肌缺血/再灌注损伤的影响

目的 观察缩醛基毛冬青提取化合物R4 对在体大鼠急性心肌缺血/再灌注损伤（I/R）的影响,并探讨其保护作用机制.方法 建立大鼠心肌缺血/再灌注模型,采用试剂盒测定再灌注40 min 后血清肌酸激酶（CK）、肿瘤坏死因子（TNF-α）、IL-1Β的水平,观察心肌梗死范围,采用凝胶电泳法测定核转录因子κB（NF-κB）的活性,采用试剂盒测定测定心肌组织超氧化物（SOD）活性及丙二醛（MDA）含量.结果 缺血20 min 再灌注40 min 后模型组及用药组的血清TNF-α、IL-1β、CK 水平明显高于假手术组,且缩醛基毛冬青提取化合物R4组及维拉帕米对照组明显低于模型组.再灌注40min后模型组及用药组的梗死范围明显增加,NF-κB 表达明显增高,且缩醛基毛冬青提取化合物R4 组及维拉帕米对照组明显低于模型组.再灌注40 min 后模型组及用药组的SOD 明显降低,MDA 明显增高,缩醛基毛冬青提取化合物R4 组及维拉帕米对照组MDA 明显低于模型组,SOD 明显高于模型组,有统计学意义.结论 缩醛基毛冬青提取化合物R4 对缺血再灌注心肌的保护作用与其显著缩小心肌梗死面积,降低肌酸磷酸激酶,降低MDA 同时提高SOD,减少心肌细胞内TNF-α、IL-1β、NF-κB 蛋白的表达有关.

Effects of MDQR4 on Acute Myocardial Ischemia Reperfusion Injury in Rats

Objective To study the effect of MDQR4 on acute myocardial ischemia reperfusion（I/R）in rats.Methods Manufac- ture the model of myocardial I/R in rats.Using kit to observe the levels of serum creatine kinase（CK）,tumor necrosis factor alpha（TNF-α）and interleukin 1β（IL-1β）.and the infarct size of each group were measured by TTC staining.And the level of NF κBwas also detected.And contentof malondialdehyde（MDA）and superoxide dismutase（SOD）in myocardial tissue were observed.Re- sults Following ischemia 20 min and reperfusion 40 min,serum concentration of TNF-α,IL-1βand CK in I/R group and medicinepretreatment group was significantly increased compared with that in sham group,and serum concentration of TNF-α,IL-1βand CKin every medicine pretreatment group was significantly lower than that in I/R group.Following ischemia 20 min and reperfusion 40min,infarct size and the expression of NF-κB in I/R group and medicine pretreatment group was significantly increased.And infarctsize and the expression of NF κB in every medicine pretreatment group was significantly lower than that in I/R group.Followingreperfusion 40 min,MDA content was significantly increased and SOD content was significantly reduced compared with that in shamgroup,and MDA content in every medicine pretreatment group was significantly lower than that in I/R group,and SOD content in ev- ery medicine pretreatment group was significantly higher than that in I/R group.Conclusion MDQR4 could reduce the infarct sizeand inhibit NF-κB activation and down regulate the expression of TNF-α,IL-1β,CK,MDA and increase the content of SOD,whichmay be one of the mechanisms of its cardioprotection.