白花前胡甲素对急性缺血再灌注大鼠心肌Fas蛋白表达及血清I-L6水平的影响

目的探讨白花前胡甲素 (Pd Ia)抗缺血再灌注损伤的机制 ,为寻找高效、低毒及安全的防治缺血再灌注损伤的药物提供理论基础。方法采用放射免疫分析测定血清白细胞介素 6(IL 6)水平 ,并用免疫组化联合计算机图像分析系统检测心肌中Fas蛋白表达。结果Pd Ia干预组IL 6水平及Fas蛋白表达指数分别由对照组的 (1 5 2 88± 1 5 2 5 )pg/mL及 (6 71± 1 47) %最大降至 (1 1 6 1 3± 1 0 45 )pg/mL及 (3 3 9± 0 92 ) % (P <0 0 1 ) ,其作用强度与硝苯地平相近。结论Pd Ia明显抑制缺血再灌注大鼠血清IL 6水平及心肌Fas蛋白表达 ,提示Pd Ia可能通过钙拮抗作用或钾通道开放作用抑制NF κB途径实现再灌注性损伤的防治。

Effect of Pd-Ia on expression of myocardial Fas protein and serum IL-6 level of ischemic reperfusion rats

Objective To provide the theoretical basis for the research on and development of higher efficancy, lower toxicity and safe drugs which could prevent and treat ischemic reperfusion, the mechanism of Pd Ia against ischemia/reperfusion injury was investigated. Methods Serum IL 6 level was measured by the radio immunization assay, and the expression of myocardial Fas protein was determined by immunohistochemo assay. Results The level of IL 6 and expression of Fas protein in Pd Ia groups were from ( 152 88± 15 25)pg/mL and (6 71±1 47)% in control of (116 13±10 45)pg/mL and (3 39±0 92)%( P <0 01), and the activity was similar to that of nefidipine. Conclusions Pd Ia inhibited obviously the serum IL 6 level and expression of Fas protein in ischemic reperfusion rats, suggesting that Pd Ia could prevent and treat ischemic reperfusion injury by blocking the calcium channel and/or opening the potassium channel and inhibiting the NF κB pathway.