地骨皮水提液对脂多糖诱导小鼠急性肺损伤的保护作用机制

Lycium chinense Water Extract Attenuates Acute Lung Injury Induced by Lipopolysaccharide in Mice

摘要:

目的: 探讨地骨皮水提物对内毒素(lipopolysaccharide, LPS)诱导小鼠的急性肺损伤(acute lung injury, ALI)保护作用.方法: 小鼠LPS(5 mg ·kg^-1 ip)复制ALI动物模型.将小鼠随机分为空白组、模型组、地塞米松组(2 mg ·kg^-1)、地骨皮水提液高、低剂量组(20,10 g ·kg^-1),腹腔注射给药.观察各组肺组织病理学改变,测量肺湿质量/干质量,支气管肺泡灌洗液(BALF)中性粒细胞百分比、肺组织中超氧化物歧化酶(SOD)、丙二醛(MDA)、炎症因子白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)含量及肺组织中SOD与MDA蛋白表达.结果: 地骨皮水提液能降低肺泡灌洗液(BALF)中炎症细胞的数目,能显著降低肺湿质量/干质量,与空白组相比, 模型组肺组织MDA含量升高(P<0.01),SOD活性降低(P<0.05), MDA蛋白水平显著升高, SOD蛋白水平显著下降(P<0.01);与模型组比较,地骨皮水提液组BALF中SOD活性显著升高(P<0.05),MDA蛋白水平降低(P<0.05),并可有效减轻LPS所致肺组织病理学变化.结论: 地骨皮水提液可减轻LPS所致急性肺组织损伤.

Abstract:

Objective:To determine the protective effect of Lycium chinense water extract (LCM) on acute lung injury(ALI) induced by lipopolysaccharide(LPS). Method: The BABL/c mice were randomly allocated into control group, LPS model group, dexamethasone (2 mg · kg^-1) group, LCM (10 g · kg^-1), and LCM (20 g · kg^-1) group by intraperitoneal injection. The bronchoalveolar lavage fluid (BALF) samples were analyzed for the concentration of numbers of neutrophilic, superoxide dismutase (SOD), malondi aldehyde (MDA), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α), and the lung samples were taken for histologic evaluation and for determination of wet-to-dry(W/D) lung weight, the protein levels of SOD and MDA were detected by Western blot analysis. Result: Pretreatment with LCM prior to the administration of intratracheal LPS significantly induced a decrease in lung wet weight/dry weight ratio, in total leukocyte number and neutrophil percent in the BALF, and in MDA activity of lung in dose-dependent manners, and in IL-6, the TNF-α in the BALF and MDA protein in lung and increased SOD protein in lung(P<0.01), compared with model the group. At the same time, compared with the blank group, pretreatment with LCM also significantly improved the SOD activity(P<0.05) and decreased the MDA activity in lung (P<0.05). Conclusion: These results showed that anti-inflammatory effects of LCM against the LPS-induced ALI.