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目的:初步探讨银杏叶提取物金纳多(Ginaton)对内毒素(lipopolysaccharide,LPS)诱导小鼠的急性肺损伤(acute lung injury,ALI)保护作用的可能机制。方法:于小鼠腹腔注射LPS(10mg/kg)复制ALI动物模型。将小鼠随机分为对照组、LPS组、Ginaton组和Ginaton+LPS组。观察各组肺组织病理学改变,测量肺湿/干重比,支气管肺泡灌洗液蛋白含量及乳酸脱氢酶(lactate dehydrogenase,LDH)活性,测量丙二醛(malondialdehyde,MDA)、一氧化氮合酶(nitric oxide synthase,iNOS)和髓过氧化物(myeloperoxidase,MPO),免疫组织化学方法检测血红素加氧酶(heme oxygenase HO-1)及iNOS蛋白表达。结果:金纳多可有效减轻LPS所致肺组织病理学变化,并降低肺湿/干重比和肺泡灌洗液中蛋白含量,降低肺泡灌洗液中LDH活性、肺组织MPO和iNOS活性,同时MDA和NO含量下降。免疫组织化学结果显示,LPS组iNOS表达上升(P<0.01),而血红素加氧酶(HO-1)蛋白表达未见明显变化;而预先给予Ginaton可显著提高HO-1的表达,降低iNOS的表达(P<0.01)。结论:Ginaton可减轻LPS所致急性肺组织损伤,其机制可能与诱导HO-1的表达,下调iNOS的表达和活性有关。
OBJECTIVE: To investigate the possible mechanism of the protective effect of Ginkgo biloba extract Ginaton against acute lung injury (ALI) in mice induced by lipopolysaccharide (LPS). METHODS: LPS (10 mg/kg) was injected intraperitoneally into mice to replicate the ALI animal model. Mice were randomly divided into control group, LPS group, Ginaton group and Ginaton+LPS group. Observe the changes of lung pathology in each group, measure lung wet/dry weight ratio, bronchoalveolar lavage fluid protein content and lactate dehydrogenase (LDH) activity, measure malondialdehyde (MDA), nitric oxide, Nitric oxide synthase (iNOS) and myeloperoxidase (MPO) were used to detect heme oxygenase (HO-1) and iNOS protein expression by immunohistochemistry. Results: Ginaton can effectively reduce the pathological changes of lung tissue caused by LPS, and reduce the wet/dry weight ratio of lung and protein content in bronchoalveolar lavage fluid, and reduce the activity of LDH in lung lavage fluid and the activity of MPO and iNOS in lung tissue. At the same time, the content of MDA and NO decreased. Immunohistochemistry results showed that the expression of iNOS in LPS group increased (P<0.01), while the expression of heme oxygenase (HO-1) protein did not change significantly; while pre-administration of Ginaton significantly increased the expression of HO-1 and decreased iNOS The expression (P<0.01). Conclusion: Ginaton can alleviate acute lung injury induced by LPS. The mechanism may be related to the induction of HO-1 expression and down-regulation of iNOS expression and activity.