Ac-SDKP 对实验性矽肺纤维化模型中肺泡Ⅱ型上皮细胞衰老信号激活的调节作用
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华北理工大学基础医学院;河北省器官纤维化重点实验室;河北省慢性病基础医学重点实验室,河北 唐山 063210

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R-33


Ac-SDKP regulates activation of senescence-related signals in alveolar type II epithelial cells in silicotic rats
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Collage of Basic Medicine, North China University of Science and Technology, Hebei Key Laboratory for Chronic Diseases, Tangshan 063000, China

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    摘要:

    目的 观察 N-乙酰基-丝氨酰-天冬氨酰-赖氨酰-脯氨酸(Ac-SDKP)对实验性矽肺纤维化进程中肺泡 II 型上皮细胞细胞衰老的作用及其机制。 方法 SPF 级 Wistar 大鼠分组为对照组、矽肺模型组和 Ac-SDKP 治疗组。肺泡 II 型上皮 MLE-12 细胞分组为空白对照组、SiO2 组、Ac-SDKP 组和 SiO2+Ac-SDKP 组。天狼星红染色显示胶原分布与沉积,免疫荧光染色检测肺组织及 MLE-12 细胞中 p21 的定位与表达;免疫印迹法检测 I 型胶原蛋白(Col I) 、p-毛细血管扩张性共济失调(ATR) 、p-p53、p-毛细血管扩张性共济失调突变激酶(ATM) 、矽肺模型组大鼠肺组织形成典型的矽结节伴胶原沉积;与矽肺模型组相比较,Ac-SDKP 治疗组大鼠肺内矽结节数量和面积显著减少。免疫荧光染色结果显示 p21 蛋白主要定位于肺泡 II 型上皮细胞。 与对照组比较,矽肺模型组肺组织内 Col I、p-ATM、p-ATR、p-p53、p21、p16 蛋白表达水平上调,而 Ac-SDKP 治疗组肺组织内 Col I、p-ATM、p- ATR、p-p53、p21、p16 蛋白表达水平下调(P<0.05) 。与空白对照组比较,SiO2 组的 MLE-12 细胞 Col I、p-ATM、p- ATR、p-p53、p21、p16 蛋白表达水平上调;与 SiO 组比较, SiO2+Ac-SDKP 组 Col I、p-ATM、p-ATR、p-p53、p21、p16 蛋白表达水平下调(P<0. 05) 。 结论 Ac-SDKP 能够通过抑制肺泡 II 型上皮细胞衰老信号的活化从而抑制胶原沉积。

    Abstract:

    Objective To explore the effects of N-acetyl-seryl-aspartyl-lysyl-proline ( Ac-SDKP) on alveolar type II epithelial cellular senescence during experimental silicosis. Methods The HOPE-MED8050 dynamic silica dust exposure control system was applied to establish a rat model of silicosis, and the experimental silicosis rats were divided into the control, dust-treated and Ac-SDKP post-treatment groups. MLE-12 cells were cultured in vitro, and the experimental cells were divided into the control, SiO2 -induction, Ac-SDKP and SiO2 + Ac-SDKP groups. Sirius red staining was used to observe collagen deposition in the lung tissue; immunofluorescence staining was used to detect the location of p21, and immunoblotting was used to detect type I collagen (Col I) expression, p-capillary dilatation ataxia mutant kinase (ATM) , p-capillary dilation ataxia (ATR) , p-p53, p21 and p16. Results The lung tissue of rats in the silicosis group could be observed with silicon nodules and collagen deposition. Immunofluorescence staining result showed that p21 was mainly localized in alveolar type II epithelial cells. Immunoblotting result showed upregulated Col I, p- ATM, p-ATR, p-p53, p21 and p16 protein expression levels in the lung tissue. Compared with those of the dust-treated group, the number and area of the silicon nodules in the lungs of the Ac-SDKP post-treated group were significantly reduced, and the protein expression levels of Col I, p-ATM, p-ATR, p-p53, p21 and p16 in the lung tissue were decreased (P<0. 05) . Compared with those of the control group, the Col I, p-ATM, p-ATR, p-p53, p21 and p16 levels in MLE-12 cells of the SiO2 -induced group were upregulated. Compared with those of the SiO2 -induced group, the Col I, p-ATM, p-ATR, p-p53, p21, p16 expression levels were downregulated in the SiO2 + Ac-SDKP group ( P< 0. 05) . Conclusions Ac-SDKP reduced collagen deposition by inhibiting activation of senescence-related signals in alveolar type II epithelial cells.

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李雅倩,张诗汇,张 乙,靳馥宇,李 田,杨欣雨,刘舒鹏,徐 洪,杨 方. Ac-SDKP 对实验性矽肺纤维化模型中肺泡Ⅱ型上皮细胞衰老信号激活的调节作用[J].中国比较医学杂志,2021,31(3):1~7.

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  • 收稿日期:2020-07-07
  • 在线发布日期: 2021-04-30
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