首页|还原型谷胱甘肽对大鼠肺成纤维细胞的影响

还原型谷胱甘肽对大鼠肺成纤维细胞的影响

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研究过量的还原型谷胱甘肽(Glutathione,GSH)对肺成纤维细胞(Lung fibroblasts,LFS)的影响,以此来探究氧化还原平衡被打破后LFS的状态和变化.提取新鲜的大鼠LFS,通过细胞活力实验、明胶酶谱法、细胞形态实验、划痕实验、细胞免疫荧光染色和蛋白质免疫印记实验,观察不同浓度的GSH对LFS的增殖、生长、迁移以及信号通路的影响.实验表明,细胞外GSH干预可以引起LFS内稳态的改变,使局部黏着斑激酶(Focal adhesion kinase,FAK)、核因子 κB(Nuclear factor kappa-B,NF-κB)、磷酸化组蛋白(Phospho-histone gamma H2 A.X,γ-H2 A.X)表达增高,但抑制细胞分泌的基质金属蛋白酶-2/9(MMP-2/9)的活力,使用过高浓度GSH干预时,其细胞的迁移、丝裂原活化蛋白激酶(p38)的表达、抑癌基因(p53)蛋白的表达被抑制.综上所述,过高的细胞外GSH可能导致LFS出现DNA损伤以及细胞衰竭并失能,从而引起肺组织病变.另外,过多抗氧化剂的使用会打破细胞内稳态平衡,并可能会对机体造成不可逆的损伤.
Effects of glutathione on rat lung fibroblasts
The purpose of this study was to investigate the effect of excessive GSH on LFS,and to ex-plore the status changes after the redox balance was broken.Fresh rat LFS were extracted and cul-tured in vitro.Cell MTT test,gelatin enzyme assay,cell morphology test,scratch test,cell immuno-fluorescence staining,and western blot were employed to observe the proliferation,growth,and mi-gration of LFS with varying concentrations of GSH as well as changes in signaling pathways.The results revealed that GSH altered intracellular homeostasis of LFS,inhibited MMP-2/9 activity,and increased the expressions of focal adhesion kinase(FAK),nuclear factor kappa-B(NF-κB),phos-pho-histone gamma H2A.X(γ-H2A.X).But the excessive GSH inhibited cell migration,p38 and p53 protein expressions.In summary,excessive GSH may induce DNA damage and exhaustion in LFS cells leading to lung problems.In addition,excessive use of antioxidants can disrupt cellular homeo-stasis and may cause irreversible damage to the body.

glutathionepulmonary fibrosislung fibroblastsredox equilibrium

秦晶莹、王车礼、孙文平、乔海燕、刘恒宇、周晓鹰

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常州大学药学院,江苏常州 213164

还原型谷胱甘肽 肺纤维化 肺成纤维细胞 氧化还原平衡

2024

常州大学学报(自然科学版)
常州大学

常州大学学报(自然科学版)

影响因子:0.459
ISSN:2095-0411
年,卷(期):2024.36(3)
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