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目的观察瘤果黑种草子总黄酮对慢性阻塞性肺病大鼠模型炎症的作用及其机制。方法采用气管内滴入脂多糖(LPS)后雾化吸入木瓜蛋白酶制备慢性阻塞性肺病模型大鼠后,分别连续灌胃给予低、高剂量的瘤果黑种草子总黄酮、水煎液及氨茶碱20 d,模型组和正常组大鼠给予蒸馏水作为对照组。观察各组大鼠的一般状况,HE染色观察肺组织的病理形态学改变,取支气管肺泡灌洗液(BALF)进行炎性细胞分类,酶联免疫分析法测定支气管肺泡灌洗液上清液白细胞介素-8、肿瘤坏死因子-α和核因子-κB的含量水平。结果瘤果黑种草子总黄酮(71.5,286 mg·kg-1)可明显改善慢性阻塞性肺病模型大鼠的一般状况,对其肺组织的病理变化有不同程度的减轻;支气管肺泡灌洗液中的巨噬细胞、中性粒细胞所占比例显著下降(P<0.01),白细胞介素-8、肿瘤坏死因子-α和核因子-κB的含量水平均降低(P<0.01)。结论瘤果黑种草子总黄酮对慢性阻塞性肺病大鼠模型炎症具有抑制作用,其机制可能与减弱炎性细胞对脂多糖的反应,抑制炎症因子的合成和释放有关。
Objective To investigate the effect and mechanism of total flavonoids of Kumia kusnezoffi on inflammation in model rats with chronic obstructive pulmonary disease. Methods Chronic obstructive pulmonary disease rats were prepared by inhalation of papain after inhalation of lipopolysaccharide (LPS) intratracheally, and then were given low and high dosages of total flavonoids, aqueous extracts and ammonia Theophylline 20 d, the model group and normal rats were given distilled water as a control group. The general condition of rats in each group was observed. The pathological changes of lung tissue were observed by HE staining. The bronchial alveolar lavage fluid (BALF) was used for inflammatory cell sorting. The level of leukocyte in bronchoalveolar lavage fluid supernatant was determined by enzyme-linked immunosorbent assay Interleukin-8, tumor necrosis factor-α and nuclear factor-κB levels. Results The results showed that the total flavonoids (71.5 and 286 mg · kg -1) of N. mongolicum could obviously improve the general condition of rats with chronic obstructive pulmonary disease and reduce the pathological changes of the lung tissue to some extent. The bronchoalveolar lavage fluid (P <0.01). The levels of IL-8, TNF-α and NF-κB in macrophages and macrophages decreased significantly (P <0.01). Conclusions The total flavonoids of Kumia kusnezoffii can inhibit the inflammation of model rats with chronic obstructive pulmonary disease. The mechanism may be related to the decrease of the reaction of inflammatory cells to lipopolysaccharide and the inhibition of the synthesis and release of inflammatory cytokines.