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出 处:《抗感染药学》2013年第1期36-39,共4页Anti-infection Pharmacy
摘 要:目的:研究丹参酮ⅡA(tanshinoneⅡA)对肠缺血再灌注的大鼠肺损伤的保护作用及其可能的作用机制。方法:采用肠系膜上动脉夹闭1h-灌注2h的方式复制肠缺血再灌注(ischemia reperfusion,IR)大鼠损伤的模型;将SD大鼠随机分为假手术组、模型组及丹参酮ⅡA(5,10,20mg/kg)组,各组于缺血前20min舌下静脉给药,测定再灌注后大鼠血清及肺组织中SOD活力、MDA和NO水平,并在光镜下观察肺组织形态学的变化。结果:模型组与假手术组相比,前者大鼠血清及肺组织中的SOD活力降低,MDA和NO水平升高,经镜检发现大鼠肺脏组织中有明显的组织形态学的损伤;丹参酮ⅡA组与模型组相比,前者呈剂量依赖性地增强大鼠SOD活力,降低MDA及NO水平,减轻大鼠肺组织中形态学的损伤。结论:丹参酮ⅡA对肠IR所致肺组织损伤有显著的剂量依赖性地保护作用,可能与其自由基清除作用、减轻中性粒细胞聚集及活化、抑制大量NO释放有关。Objective: To study the protections oftanshinone Ⅱ A on lungs injury induced by intestinal ischemia re- perfusion(IR) in rats and its possible mechanism. Methods:The IR rats model was established by occluding the superi- or-mesenteric artery(SMA) for 1 h, and followed by reperfusion for 2 h.SD rats were randomly divided into five groups: Sham group, Model group, Tan Ⅱ A groups (Tan Ⅱ A 5,10 and 20 mg/kg). Each group was administered by sublingual vein at 20 min before ischemia. SOD activity, MDA and NO levels in serum and lungs issue were determined. Histomorphology changes of lungs injury tissue were observed with light microscope. Results: Compared with sham group, SOD activity was decreased, MDA and NO levels were increased and histomorphology of lungs was destroyed obviously by microscopy examination in serum and lungs issue in model group. Compared with model group, Tan ⅡA could dose-dependently increase SOD activity and decrease MDA and NO levels in serum and lungs tissue. Also, Tan ⅡA could dose-dependently attenuate lungs tissue injury. Conclusion: Tan ⅡA can dose-dependently protect lungs significantly and attenuate intestinal IR injury. These protective effects are related to their anti-free-radical actions with diminishing the aggregation and activation of polymorphonuclear neutrophile(PMN) and inhibiting the release of NO.
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