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目的:观察泻肺平喘灵及其拆方对“肺合大肠”模型大鼠血清内毒素(ET)和肿瘤坏死因子-α(TNF-α)变化的影响。方法:70只SD大鼠随机分为7组(正常组、模型组、解扎组、三拗组、三通组、三活组、泻肺平喘灵组),每组10只。采用直肠体外不全结扎法制备“肺合大肠”动物模型,造模3 d后处死模型组;三拗组以三拗汤3.92 g.kg-1 ig;三通组以三通方7.11 g.kg-1 ig;三活组以三活方10.54 g.kg-1 ig;泻肺平喘灵组以泻肺平喘灵16.66 g.kg-1 ig,正常组和解扎组以10 mL.kg-1生理盐水ig,3d后处死大鼠。观察大鼠血清ET和TNF-α的改变,观察泻肺平喘灵及其拆方的干预效果。结果:模型组大鼠造模后血清ET和TNF-α水平均明显升高(P<0.01),解扎组、泻肺平喘灵及其拆方组均降低,与模型组比较有非常显著性差异(P<0.01);泻肺平喘灵及其拆方组与解扎组比较也有显著性差异(P<0.01);部分药组之间呈协同的作用趋势。结论:泻肺平喘灵及其拆方能够降低模型大鼠血清ET和TNF-α水平,从而保护肺组织,减轻肺部病变,有效阻断内毒素血症对模型大鼠组织的损伤。
Objective: To observe the effects of Xiefei Pingchuan and its disassembled formulas on the changes of serum endotoxin (ET) and tumor necrosis factor-α (TNF-α) in rats with pulmonary interstitium. Methods: Seventy SD rats were randomly divided into 7 groups (normal group, model group, Jieza group, Sanan group, SanTong group, SanHuo group and XieFeiPengGanLing group) with 10 in each group. The animal model of “lung combined with large intestine” was prepared by rectal in vitro ligation and the model group was sacrificed 3 days after the model was established. The Sanmao group was 3.92 g.kg-1 ig with Sanan soup, the tee group with 7.11 g . kg-1 ig; Sanshuo group 10.54 g.kg-1 ig Sanhuo Fang; Xiefei Ping Chuanling group to Xiefei Pinggan 16.66 g.kg-1 ig, normal group and Jieza group 10 mL. kg-1 normal saline ig, 3d rats were sacrificed. The changes of serum ET and TNF-α in rats were observed to observe the intervention effect of Xiefei Pingchuanling and its disassembled prescriptions. Results: The levels of serum ET and TNF-α in the model group were significantly increased (P <0.01), and the Jieza group, Xiefei Pingchuan and its disassembled group were all lower than the model group (P <0.01). There was also a significant difference between Xiegan Pingchuan and its disassembled group and Jieza group (P <0.01). Some drug groups showed a synergistic effect. Conclusion: Xiegan Pingchuan and its disassembled prescriptions can reduce the levels of serum ET and TNF-α in model rats, thus protecting the lung tissue, alleviating the pathological changes of the lungs and effectively blocking the damage of endotoxemia to the model rats.