β-葡聚糖抑制大鼠硅肺纤维化损伤的机制研究

发布时间：2018-03-29 17:05

本文选题：β-葡聚糖　切入点：氧化应激　出处：《安徽医科大学学报》2017年12期

【摘要】：目的探讨β-葡聚糖通过对氧化应激的调节,抑制大鼠硅肺纤维化的作用及其机制。方法采用动式染尘法制作大鼠硅肺模型,实验分组为:对照组、模型组、β-葡聚糖前处理组、β-葡聚糖后处理组。HE染色观察肺组织病理形态,检测各组大鼠肺组织及血清的丙二醛(MDA)表达、过氧化氢酶(CAT)以及还原型谷胱甘肽(GSH)表达;采用Western blot法检测肺组织内I型胶原、α-平滑肌肌动蛋白(α-SMA)、硫氧还蛋白-1(TRX-1)的表达。结果与对照组相比,模型组有典型的矽结节形成,α-SMA阳性染色明显,而β-葡聚糖前、后处理组均能够显著抑制大鼠肺纤维化程度。与对照组相比,模型组肺组织、血清中MDA含量明显上调,而血清中CAT及肺组织中GSH含量增高,同时伴有I型胶原、α-SMA蛋白水平的上调和TRX-1蛋白水平的下调(P0.05);而予以β-葡聚糖前处理和后处理,均能够显著抑制二氧化硅引起的上述病变,差异有统计学意义(P0.05)。结论β-葡聚糖可能通过上调TRX-1表达,拮抗氧化应激损伤,从而抑制硅肺纤维化的发生与发展。
[Abstract]:Objective to investigate the effect and mechanism of 尾 -glucan on inhibiting silicosis fibrosis in rats by regulating oxidative stress. Model group, 尾 -glucan pretreatment group and 尾 -glucan post-treatment group. He staining was used to detect the expression of malondialdehyde (MDAs), catalase (CAT) and glutathione (GSH) in lung tissue and serum of rats in each group. The expression of type I collagen and 伪 -smooth muscle actin (伪 -SMA-1) in lung tissue was detected by Western blot method. Results compared with the control group, the model group had typical silicon nodule formation, 伪 -SMA positive staining and 尾 -glucan. Compared with the control group, the serum MDA content in the model group was significantly increased, while the CAT in serum and the GSH content in the lung tissue were increased in the post-treatment group. At the same time, type I collagen, 伪 -SMA protein and TRX-1 protein were up-regulated and down-regulated P0.05.The pretreatment and post-treatment with 尾 -glucan could significantly inhibit the above pathological changes induced by silica. Conclusion 尾 -glucan may inhibit the occurrence and development of silicosis by upregulating the expression of TRX-1 and antagonizing oxidative stress injury.
【作者单位】：华北理工大学医学实验研究中心老年医学国际科技合作基地;
【基金】：国家自然科学基金(编号:81673119) 唐山市科技计划项目(编号:14160201B) 河北省卫计委医学科学研究项目(编号:20160717) 华北理工大学大学生创新项目(编号:X2016215)
【分类号】：R135.2

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