疏风解毒胶囊对于内毒素诱导大鼠急性肺损伤模型中MAPK/NF-κB通路的抑制作用

Shufeng Jiedu Capsule regulates LPS-induced acute lung injury via inhibiting MAPK/ NF-κB pathways

目的:观察疏风解毒胶囊对内毒素(LPS)致大鼠肺损伤的保护作用,并探讨其对于MAPK/NF-κB Signaling通路的影响。方法:以腹腔注入LPS 10mg/kg制备成急性肺损伤模型,疏风解毒胶囊治疗组每天灌胃给药疏风解毒胶囊100mg/kg,观察第1、3、5、7天各组的血气分析、乳酸、肺组织HE染色病理学观察、肺组织白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)免疫荧光标记后激光共聚焦显影、IL-1β、P-选择素、转化生长因子β(TGF-β)、角质细胞的趋化因子(KC)、激活蛋白Ap-1(C-Jun/AP-1)浓度、核因子-κB(NF-κB)的mRNA表达水平的影响。结果:疏风解毒胶囊治疗组可明显缓解LPS诱导大鼠急性肺损伤的血气低氧及乳酸升高,其肺组织病理炎性渗出程度较轻。疏风解毒胶囊治疗组大鼠肺组织的IL-1β、TNF-α、P-选择素、TGF-β、KC、C-Jun/AP-1水平较LPS模型组有明显下降(P<0.05),其肺组织NF-κB mRNA表达明显低于LPS模型组(P<0.05)。结论:疏风解毒胶囊可抑制LPS诱导的炎性反应,减轻内毒素导致的肺损伤反应;其对于炎性反应的抑制机制可能与抑制MAPK/NF-κB Signaling通路、下调NF-κB mRNA的表达有关。

Objective： To observe the protective effects of Shufeng Jiedu Capsule on SD mice with acute lung injury induced by LPS and explore the effect of MAPK/NF-κB signaling pathway. Methods： The mice were intraperitoneal injected with LPS 10mg/kg in order to induce the model of acute lung injury. The rats in Shufeng Jiedu Capsule treatment group were given a gavage of Shufeng Jiedu Capsule 100 mg/kg. At 1st day, 3rd day, 5th and 7th day, each groups were observed pathological manifestations; confocal imaging examination of lung tissue after IL-1β, TNF-α immunofluorescence, the level of IL-1β, P-selectin, TGF-β, keratinoeyte-derived chemokine （KC） and C-Jun/AP-1; mRNA expression of nuclear factor κB （NF-κB）. Results： Shufeng Jiedu Capsule significantly alleviated the extent of pulmonary inflammation. In the Shufeng Jiedu Capsule treatment group, IL-1β, TNF-α, P-selectin, TGF-β, KC and C-Jun/AP-1 levels of lung tissue were lower than that in LPS induced model group （P〈0.05）, In the Shufeng Jiedu Capsule treatment group, NF-κB mRNA expression of the lung tissue was significantly lower than that in the LPS induced model group （P〈0.05）. Conclusion： Shufeng Jiedu Capsule could reduce the reaction of LPS-induced lung inflammation, the mechanism of inhibition of inflammation might be associated with inhibiting the MAPK/NF-κB pathways and downregulation of the expression of NF-κB mRNA.