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[目的]研究丹参酮ⅡA对急性胰腺炎相关性肺损伤(APALI)的干预作用,并探讨其作用机制。[方法]SD大鼠随机分为3组:假手术(对照)组、APALI组及丹参酮ⅡA干预组,应用5%牛磺胆酸钠逆行胰胆管注射建立大鼠APALI动物模型,观察各组肺组织中肺脏湿干重比、髓过氧化物酶(MPO)的活性、肿瘤坏死因子-α(TNF-α)、白细胞介素1β(IL-1β)水平、细胞间黏附分子(CAM)的表达,同时比较各组肺组织损伤积分。[结果]与假手术对照组比较,APALI组肺组织肺脏湿干重比,MPO活性,TNF-αI、L-1β水平,ICAM的表达及肺组织病理损伤积分均显著增高(均P<0.05);丹参酮ⅡA干预组与APALI组相比,肺组织肺脏湿干重比,MPO活性,TNF-αI、L-1β水平,ICAM的表达及肺组织病理损伤积分均显著降低(均P<0.05);[结论]丹参酮ⅡA可以下调炎性因子的表达而减轻APALI的炎症反应。
[Objective] To study the intervention effect of tanshinone Ⅱ A on acute pancreatitis-associated lung injury (APALI) and its mechanism. [Methods] SD rats were randomly divided into 3 groups: sham operation (control) group, APALI group and tanshinone ⅡA intervention group. The APALI model was established by injecting 5% sodium taurocholate into pancreaticobiliary duct. The ratio of lung wet to dry weight, the activity of myeloperoxidase (MPO), the level of tumor necrosis factor-α (TNF-α), the level of interleukin 1β (IL-1β) and the expression of intercellular adhesion molecule , While comparing the lung injury scores of each group. [Results] The lung wet / dry weight ratio, MPO activity, TNF-αI, L-1β level, ICAM expression and lung injury pathological scores of lungs in APALI group were significantly higher than those in sham operation control group (all P <0.05) Compared with APALI group, the lung wet / dry weight ratio, MPO activity, TNF-αI and L-1β levels, ICAM expression and lung injury pathological scores were significantly decreased in tanshinone ⅡA intervention group (all P <0.05); [Conclusion] Tanshinone IIA can reduce the inflammatory response of APALI by down-regulating the expression of inflammatory cytokines.