野马追各化学部位对小鼠急性肺损伤的保护作用

目的:比较野马追各化学部位对脂多糖(LPS)诱导的小鼠急性肺损伤(ALI)的保护作用及其药理机制。方法:将昆明种小鼠随机分为对照组、LPS组、给药组和阳性组,连续灌胃给药1周后,采用气管滴注脂多糖法复制小鼠ALI模型,造模6小时后,测定小鼠肺湿/干重比(Lung W/D r at i o),肺泡灌洗液(BALF)中一氧化氮(NO)和蛋白质含量以及血清中补体C3(C3)和C3c含量;24小时后检测肺组织匀浆中髓过氧化酶(MPO)和超氧化物歧化酶(SOD)活性以及BALF中肿瘤坏死因子α(TNF-α)、白介素6(I L-6)和白介素1β(I L-1β)含量,观测HE和免疫组化染色后小鼠肺组织病理改变。结果:野马追提取物及其氯仿、乙酸乙酯、正丁醇层、水层、野马追黄酮部位、野马追倍半萜部位均能降低脂多糖诱导小鼠的炎症因子TNF-α、I L-6水平,提高SOD活性并抑制MPO活性;野马追水层能减轻LPS诱导ALI小鼠肺水肿和肺组织病理改变,减少BALF中NO和蛋白质含量,提高肺组织中SOD活性并抑制MPO活性,降低BALF中TNF-α、I L-6和I L-1β含量,减少血清中C3含量并改善肺组织中补体片段C3c沉积。结论:野马追各化学部位对小鼠急性肺损伤的作用机制与抑制炎症因子,降低补体C3水平和抗氧化有关。

Protective Effects of Various Chemical Fractions of YeMaZhui on Acute Lung Injury in Mice

Objective:To compare the protective effects and pharmacological mechanisms of various chemical fractions of Y eMaZhui (eupatorium lindley anum DC.) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. Methods:The Kunming mice were randomly divided into the control group, LPS group, the administration group and the positive group. After intragastric administration for one week, the ALI mice models were replicated by intratracheal instillation of lipopolysaccharide. Lung wet/dry weight ratio (Lung W/D ratio), contents of nitric oxide (NO) and protein in bronchoalveolar lavage fluid (BALF) as well as complement 3 (C3) and C3c in serum were determined in six hours after the molding. 24 hours later, the activities of myeloperoxidase (MPO) and superoxide dismutase (SOD) in lung tissue homogenates, as well as the contents of tumor necrosis factor-α(TNF-α), interleukin 6 (IL-6) and interleukin 1β (IL-1β) in BALF were detected. Besides, pathological changes of lung tissue in mice were observed after HE and immunohistochemical staining. Results:Extract of YeMaZhui, chloroform, ethyl acetate, n-butanol and water layer, as well as flavonoids sites and sesquiterpene sites of YeMaZhui could reduce the levels of inflammatory factors TNF-αand IL-6, increase the activity of SOD and inhibit the activity of MPO;water layer of Y eMaZhui can reduce the pulmonary edema and pathological changes of lung tissue of LPS-induced ALI mice, and decrease the contents of NO and protein in BALF. At the same time, it can also increase the activity of SOD in lung tissue and restrain the activity of MPO, lower the contents of TNF-α, IL-6 and IL-1βin BALF and C3 in serum, and improve the deposition of complement fragment C3c in lung tissue. Conclusion:Action mechanism of various che-mical fractions of YeMaZhui on acute lung injury in mice is related to inhibiting inflammatory factors, reducing the levels of complement C3 and antioxidation.