银杏叶总黄酮对脂多糖所致小鼠急性肺损伤的保护作用

目的 探讨银杏叶总黄酮对急性肺损伤(aute lung injury,ALI)的防治作用及其作用机制.方法 50只雄性ICR小鼠随机分为正常对照组、ALI模型组和银杏叶总黄酮(total ginkgo flavone glycosides,TFG)低、中、高剂量组,每组10只,采用脂多糖(lipopolysaccharide,LPS)诱导小鼠ALI模型,给药后测定小鼠肺湿/干重比,伊文斯蓝法检测肺血管通透性,检测肺组织匀浆中超氧化物歧化酶(superoxide dismutase,SOD)活力和丙二醛(malondialdehyde,MDA)含量,观察各组肺组织的病理变化,免疫组织化学染色技术检测肺组织中核因子κB(nuclear factor-kappaB,NF-κB)的表达.结果 与ALI模型组相比,TFG高剂量组可降低升高的肺湿/干重比(P＜0.05),降低肺血管的通透性;与ALI模型组比较,TFG组肺组织匀浆中SOD活力升高、MDA含量下降(P值均＜0.01);HE染色显示ALI模型组气道管腔内有大量炎性细胞聚集,肺泡内有大量蛋白水肿液,TFG各给药组病变较ALI模型组减轻;ALI模型组NF-κB表达显著增加(P＜0.01),TFG治疗组则明显减少.结论 TFG对LPS所致ALI小鼠有明显的保护作用,其机制可能与其提高抗氧化能力,阻断NF-κB的表达有关.

Protective effect of total ginkgo flavone glycosides in lipopolysaccharide-induced acute lung injury mice

Objective To investigate the effect of total ginkgo flavone glycosides(TFG) on acute lung injury(ALl) and its mechanism in mice. Methods Fifty male ICR mice were randomly divided into control group,ALI group and TFG 10,20,40 mg/kg groups, the ALI model was established by lipopolysaccharide (LPS) i. p. Lung dry weight and wet weight percentage were detected. Evans blue spectrophotometry were used for determination of pulmonary vascular permeability and superoxide dismutase (SOD) activity,malondialdehyde(MDA) content in lung tissue were measured. The change of pathology was observed and the expression of nuclear factor-kappaB(NF-κB) protein in lungs was detected by immunohistochemical staining. Results Compared with ALI group,TFG induced a decrease in lung weight/dry weight ratio in 40 mg/kg group,and significantly decreased the pulmonary vascular permeability. Compared with ALI group,SOD activity was increased remarkably,and MDA content was decreased in lung tissue of TFG group(all P＜0.01). HE staining showed that lung tissues in model group had obvious histopathological signs of phlegmasia,and lots of protein in alveolus were observed. In contrast, the inflammatory reactions in TFG groups were much less. Expression of GATA-3 was obviously increased in model group,while the expression decreased notably in TFG treated group. Conclusions TFG plays a protective effect in ALI mice, whose mechanism may be explained by TFG in increasing antioxidant capacity and blockade NF-κB expression.