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机构地区:[1]仙桃市第一人民医院神经内科,湖北省仙桃市433000
出 处:《医学分子生物学杂志》2016年第4期218-222,共5页Journal of Medical Molecular Biology
摘 要:目的:研究中和IL-17 A对博莱霉素( bleomycin, BLM)诱导的肺纤维化小鼠肺组织Bax/Bcl-2表达的影响。方法将小鼠分别分成生理盐水组、 BLM组、 IL-17 A抗体组和IL-17 A抗体对照组,各30只,利用HE染色、 Masson三色胶原纤维染色检测小鼠肺组织纤维化程度,免疫组化方法检测小鼠肺组织Bax/Bcl-2的表达。结果从生理盐水组、到IL-17 A抗体组、再到BLM组和IL-17 A抗体对照组,小鼠肺组织肺泡炎症程度、肺泡壁的增厚情况以及肺泡壁的纤维化程度逐渐加重,差异有显著性意义(P<0.01); BLM组和IL-17 A抗体对照组间无明显差异(P>0.05)。4组间Bax蛋白、 Bcl-2蛋白的表达也逐渐加重,差异均有统计学意义( P<0.01和P<0.05)。 BLM组与抗体对照组间Bax、 Bcl-2的表达均无显著差异(P>0.05)。结论 BLM可通过IL-17 A来诱导肺纤维化的形成,肺纤维化时肺实质细胞凋亡增多,而中和IL-17 A可通过调节Bax/Bcl-2的表达来抑制肺组织气道上皮的凋亡、达到抑制肺纤维化的目的。Objective To investigate the effect of anti-IL-17 A on the expression of Bax/Bcl-2 in pulmonary tissues of mice with bleomycin ( BLM) -induced pulmonary fibrosis.Methods The mice were divided into saline group, BLM group, anti-LI-17A group and anti-IL-17A control group ( n=30 each) .Hematoxylin-eosin ( HE) staining and Masson’ s Trichrome staining were used to detect the fibrosis of pulmonary tissues in mice and immunohistochemistry to measure the expression of Bax/Bcl-2 in pulmonary tissues.Results The inflammation of the alveoli, the thickening and the fibrosis of the alveolar wall gradually deteriorated from saline group, anti-IL-17 group, BLM group to anti-IL-17 control group, and there were significant differences between groups except be-tween BLM group and anti-IL-17A control group (P〈0.05) .The expression of Bax/Bcl-2 protein was significantly lower in the anti-IL-17 group than in other three groups ( P〈0.01 or P〈0.05 ) .No significant difference was found in the expression of Bax/Bcl-2 protein between BLM group and anti-IL-17 control group ( P〉0.05) .Conclusion BLM can induce the formation of pulmonary fi-brosis, which causes the increase in the apoptosis of pulmonary parenchyma cells.Anti-IL-17 can suppress the apoptosis of the airway epithelial cells and therefore the pulmonary fibrosis by regulating the expression of Bax/Bcl-2.
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