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目的:观察芪冬活血饮对脂多糖所致大鼠急性肺损伤(ALI)的保护作用并探讨其作用机制。方法:50只SD大鼠随机分为空白组,模型组,芪冬活血饮高、中、低剂量组5组,每组10只。气道内滴注脂多糖建立ALI模型。治疗组芪冬活血饮灌胃,空白组及模型组0.9%氯化钠溶液代替。造模后24h处死大鼠收集标本。结果:芪冬活血饮减少肺损伤大鼠肺泡结构破坏、肺水肿及炎性细胞浸润。ALI大鼠TNF-α、IL-1β、IL-10水平增高(P<0.01),芪冬活血饮降低TNF-α、IL-1β水平,升高IL-10水平,高剂量组与低剂量组比较差异有统计学意义(P<0.01)。ALI大鼠NF-κBp65、Cav-1蛋白及m RNA表达增加(P<0.01),芪冬活血饮可减少其表达,免疫组化积分及m RNA相对表达高剂量组低于低剂量组,比较差异均有统计学意义(P<0.01)。结论:芪冬活血饮对LPS诱导的ALI有保护作用,其机制与抑制Cav-1/NF-κBp65炎性反应信号通路有关。
Objective: To observe the protective effect of Qi Dong Huoxue Yin on lipopolysaccharide-induced acute lung injury (ALI) in rats and its mechanism. Methods: Fifty Sprague-Dawley rats were randomly divided into blank group, model group and Qidudonghuoxueyin high, medium and low dose groups of 5, with 10 rats in each group. Instillation of lipopolysaccharide in the airway to establish ALI model. Treatment group Qidudong Huoxue Yin gastric perfusion group and model group 0.9% sodium chloride solution instead. Rats were sacrificed 24h after modeling to collect the specimens. Results: Qi Dong Huoxue Yin can reduce alveolar structural damage, pulmonary edema and inflammatory cell infiltration in rats with lung injury. The levels of TNF-α and IL-1β in ALI rats were significantly increased (P <0.01), and Qidudonghuoxueyin could reduce the levels of TNF-α and IL-1β and IL-10 levels in high-dose and high-dose groups The difference was statistically significant (P <0.01). The expression of NF-κBp65, Cav-1 protein and m RNA in ALI rats increased (P <0.01). Qidudonghuoxue Decoction could reduce its expression, and the expression of immunohistochemical score and m RNA in high dose group was lower than that in low dose group The differences were statistically significant (P <0.01). Conclusion: Qidushenhuoxue Decoction can protect ALI induced by LPS, and its mechanism is related to inhibition of Cav-1 / NF-κBp65 inflammatory response signal pathway.