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目的探讨丹参酮ⅡA对重症急性胰腺炎(severe acute pancreatitis,SAP)肺损伤(lung iniury,LI)大鼠的改善作用及其可能机制。方法予SD大鼠注射牛磺胆酸钠建立SAP模型(简称SAP组),并在此基础上给予丹参酮ⅡA(sodium tanshinoneⅡA sulfonate,STS)干预(简称STS组),同时设立假手术对照组(简称SO组),每组24只大鼠。观察各组大鼠的生存状态、肺脏湿干重比、MPO试剂盒测定肺组织髓过氧化物酶(MPO)活性、Hofbuaer方法测定肺组织病理损伤、采用E LISA方法测定肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(lL-1β)、采用免疫组化方法测定细胞间黏附分子-1(ICAM-1)表达水平。结果 SAP组大鼠生存状态恶化,肺脏湿干重比、肺组织MPO活性、肺组织病理损伤评分以及细胞因子TNF-α、IL-1β和ICAM-1均明显高于SO组,而与SAP组比较,STS组大鼠生存状态好转,肺脏湿干重比、肺组织MPO活性、肺组织病理损伤评分及TNF-α、IL-1β、ICAM-1水平均明显下降,差异均有统计学意义(P<0.05)。结论丹参酮ⅡA对大鼠SAPLI有明显改善作用,其机制可能与改变肺脏细胞因子水平、减轻肺脏炎性细胞浸润有关。
Objective To investigate the effect of tanshinone ⅡA on lung injury in rats with severe acute pancreatitis (SAP) and its possible mechanism. Methods SD rats were injected with sodium taurocholate (SAP) to establish the SAP model. On the basis of this, the rats were given STS (STS) intervention and STS (sham operation group) SO group), 24 rats in each group. The survival of rats in each group was observed, the wet / dry weight ratio of lungs was measured, the activity of MPO in lung tissue was determined by MPO kit, the pathological damage of lung tissue was determined by Hofbuaer method, the level of tumor necrosis factor- TNF-α) and interleukin-1β (IL-1β), and the expression of intercellular adhesion molecule-1 (ICAM-1) was detected by immunohistochemistry. Results The survival status, wet lung weight ratio, lung tissue MPO activity, lung histopathological damage score, cytokines TNF-α, IL-1β and ICAM-1 in SAP group were significantly higher than those in SO group Compared with the control group, STS group had better survival status, wet and dry lung weight ratio, lung tissue MPO activity, pathological damage score of lung tissue and TNF-α, IL-1β and ICAM-1 levels were significantly decreased, the differences were statistically significant P <0.05). Conclusion Tanshinone ⅡA can significantly improve SAPLI in rats, and its mechanism may be related to changing the level of cytokines in the lungs and alleviating inflammatory cell infiltration in the lungs.