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目的观察1,25-二羟维生素D3[1,25-(OH)2D3]对支气管哮喘(简称哮喘)小鼠气道重塑及其肺组织中基质金属蛋白酶9(matrix metalloprotease-9,MMP-9)表达的影响,探讨1,25-(OH)2D3在哮喘治疗中的作用。方法BALB/c小鼠随机分为对照组、哮喘组及1,25-(OH)2D3组。卵白蛋白致敏和激发建立慢性哮喘小鼠模型;HE染色观察各组气道结构改变情况;采用计算机图像分析系统评价各组气道重塑情况;采用RT-PCR法检测各组的MMP-9mRNA表达水平。结果①HE染色提示哮喘组与对照组相比出现炎性细胞浸润增多、上皮细胞脱落及平滑肌细胞层增厚等气道重塑改变,而1,25-(OH)2D3组可部分逆转上述病理改变;②1,25-(OH)2D3组的支气管内壁厚度、平滑肌层厚度和平滑肌细胞核数显著低于哮喘组,但仍高于对照组(P<0.05);③1,25-(OH)2D3组肺组织MMP-9mRNA表达水平均明显低于哮喘组,但仍高于对照组(P<0.05)。结论1,25-(OH)2D3干预可显著减轻慢性哮喘气道重塑的病理改变;并可通过部分抑制肺内MMP-9的表达来延缓气道重塑进程。
Objective To investigate the effects of 1,25-dihydroxyvitamin D3 (1,25- (OH) 2D3] on airway remodeling and the expression of matrix metalloproteinase-9 (MMP-9) in bronchial asthmatic mice 9) expression, to explore the role of 1,25- (OH) 2D3 in the treatment of asthma. Methods BALB / c mice were randomly divided into control group, asthma group and 1,25- (OH) 2D3 group. Ovalbumin sensitized and challenged to establish a chronic asthmatic mouse model; HE staining was used to observe the change of airway structure in each group; computer image analysis system was used to evaluate the airway remodeling; RT-PCR was used to detect the expression of MMP-9mRNA in each group Level. Results (1) HE staining suggested that the airway remodeling in the asthma group increased compared with the control group, and the epithelial cells shedding and the thickening of the smooth muscle cell layer changed. However, the changes of the pathological changes were partially reversed in the 1,25- (OH) 2D3 group ; ② In the 1,25- (OH) 2D3 group, the thickness of the bronchus wall, the thickness of the smooth muscle layer and the number of smooth muscle cells were significantly lower than those in the asthma group (P <0.05); ③1,25- (OH) The expression of MMP-9mRNA in the tissue was significantly lower than that in the asthma group, but still higher than that in the control group (P <0.05). Conclusions 1,25- (OH) 2D3 can significantly reduce the pathological changes of airway remodeling in chronic asthma, and delay the process of airway remodeling by partially inhibiting the expression of MMP-9 in the lung.