中文摘要：

目的研究芒果苷对香烟烟熏所致慢性支气管炎大鼠超氧化物歧化酶同工酶表达的调控作用及支气管上皮细胞超微结构的保护作用与抗炎作用。方法以香烟烟熏建立慢性支气管炎大鼠模型。分别以实时荧光逆转录-聚合酶链反应与酶联免疫分析检测肺组织超氧化物歧化酶1、超氧化物歧化酶2、超氧化物歧化酶3的mRNA与蛋白表达,酶联免疫分析测定肺组织白细胞介素-1、肿瘤坏死因子-α、丙二醛,肺组织透射电子显微镜观察支气管上皮细胞超微结构,肺组织HE染色病理形态观察。结果香烟烟熏导致大鼠肺组织超氧化物歧化酶1、超氧化物歧化酶2、超氧化物歧化酶3的表达下调。芒果苷不能拮抗肺组织超氧化物歧化酶1、超氧化物歧化酶2表达下调,但显著抑制超氧化物歧化酶3表达下调,明显降低肺组织白细胞介素-1、肿瘤坏死因子-α、丙二醛水平,保持支气管上皮细胞超微结构完整性,显著减轻慢性支气管炎症。结论芒果苷可显著减轻香烟烟熏引起的慢性支气管炎症,保护支气管上皮细胞,此作用可能并不仅依赖于芒果苷对肺组织超氧化物歧化酶3表达下调的拮抗作用。

英文摘要：

OBJECTIVE This research was designed to investigate the regulation of mangiferin on superoxide dismutase （SOD） isozyme expressionin rats with eigarettesmoke-induced chronic bronchitis, plus withthe protection on bronchial epithelial cellsultrastructure and anti-inflammatory action. METHODS The rat model with chronic bronchitis was established by cigarette smoke. Real-time fluorescence RT-PCR was executed for evaluating the SOD1, SOD2 and SOD3 gene expression in lung tissue, and enzyme-linked im- muno sorbent assay （ELISA） for SOD1, SOD2 and SOD3 protein level. As well, interleukin-1 （ IL-1 ）, tumor necrosis factor-α （ TNF- α） and malondialdehyde （MDA） level in lung tissue were detected by ELISA. Furthermore, the bronchial epithelial eellsuhrastructure was observed under transmission electron microscopy. The histopathological images was obtained by lung tissue HE staining slides. RESULTS The cigarette smokeresulted in a markedly down-regulation expressions of SOD1, SOD2 and SOD3 in lung tissue. The down-regulation expressions of SOD1 and SOD2 in lung tissue cannot be antagonized by mangiferin. However, mangiferin significantly inhibited the down-regulation of SOD3, and markedly decreased IL-1, TNF-α and MDA. Furthermore, the structural completeness of the bronchial epithelial cellsuhrastructure was maintainedin a good attitude by mangiferin, while the greatly reduced chronic bronchitis was found. CONCLUSION Mangiferin can obviously reduce the chronic bronchitis induced by cigarette smoke and keep the bronchial epithelial ceils from damage. The protective action might not rely only on anantagonistic action on down-regulated SOD3 expression in lung tissue by mangiferin.