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作 者:刘文霞[1] 树俊莲[2] 曹军平[3] 李莉[2] 马毅[4]
机构地区:[1]武警北京总队第三医院特诊科,100141 [2]中国武警总医院药剂科,100039 [3]中国武警总医院消毒供应科,100039 [4]中国武警总医院磁共振科,100039
出 处:《医学研究杂志》2016年第3期157-160,共4页Journal of Medical Research
摘 要:目的探讨丹皮酚(PA)对心肌缺血再灌注(MI/R)损伤的保护作用。方法通过结扎左冠脉前降支30min再灌注2h建立MI/R大鼠模型,随机分为假手术组、模型组、PA组(10、20、40mg/kg),每组10只,各组于术前1周开始灌胃给药,每天1次。再灌注后取血清,采用比色法测定肌酸激酶(CK)和乳酸脱氢酶(LDH)活性,ELISA法测定肿瘤坏死因子-α(TNF-α)和白介素-1β(IL-1β)水平;取心脏,染色法测定心肌梗死面积;取心肌匀浆,比色法测定髓过氧化物酶(MPO)活力。结果 PA高剂量可明显缩小MI/R损伤大鼠的心肌梗死面积,与模型组比较,差异有统计学意义(P<0.05);与模型组比较,PA各剂量可显著降低血清CK活性(P<0.05或P<0.01),PA高、中剂量可明显降低LDH活性(P<0.05或P<0.01);PA各剂量组心肌MPO活力明显降低,与模型组比较,差异均有统计学意义(P<0.05或P<0.01);PA各剂量组血清TNF-α和IL-1β水平均比模型组显著降低(P<0.05或P<0.01)。结论 PA预处理可抑制中性粒细胞浸润、减少炎性细胞因子的释放,实现对MI/R所致心肌损伤的保护作用。Objective To investigate the protective effects of paeonol (PA) against myocardial ischemia/reperfusion (MI/R) injury in rats. Methods Rat model of MI/R injury was established by coronary artery ligation for 30 min followed by 120min reperfusion. Then rats were randomly divided into five groups (n=10): sham group, model group, model+10mg/kg PA group, model+20mg/kg PA group and model + 40mg/kg PA group. PA was orally administered once a day for 7 days pre-operation. The CK and LDH activities in sera were detected by chromatometry and the levels of TNF-α and IL-1β in sera were examined by ELISA after the reperfusion. The size of myocardial infarction was measured by NBT staining. The MPO activity, an index of neutrophil infiltration, in heart homogenate was determined by chromatometry. Results PA (40mg/kg) significantly reduced the size of myocardial infarction comparing to that of model group (P〈0.05). The CK activities in all PA groups and LDH activities in PA groups (20 and 40mg/kg) were significantly lower than those of model group (P〈0.05 or P〈0.01). PA evidently reduced the MPO activity in heart homogenate comparing to that of model group (P〈0.05 or P〈0.01). The TNF-α and IL-1β levels in sera of PA groups were significantly lower than those of model group (P〈0.05 or P〈0.01). Conclusion The effectiveness of PA pretreatment in MI/R injury appears to be associated with the inhibition of neutrophil infiltration and expression of inflammatory cytokines.
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