医学分子生物学杂志 ›› 2025, Vol. 22 ›› Issue (4): 319-324.doi: 10.3870/j.issn.1672-8009.2025.04.003

• 论著 • 上一篇    下一篇

Linc279227 调控 PINK1 / Parkin 介导的线粒体自噬影响糖尿病肾病小鼠肾损伤研究 #br#

  

  1. 郴州市第四人民医院1内分泌科,2肾内科 湖南省郴州市, 423300 2湘西自治州人民医院肾内科 湖南省吉首市, 416000
  • 出版日期:2025-07-31 发布日期:2025-07-18
  • 基金资助:
    湖南省自然科学基金 (No. 2024JJ7556)

Effect of Linc279227 on Renal Injury in Diabetes Nephropathy Mice via PINK1 / Parkin Mediated Mitochondrial Autophagy #br#

  1. 1Department of Endocrinology,2 Department of Nephrology, the Fourth People’s Hospital of Chenzhou City, Chenzhou, Hunan, 423300, China 2 Department of Nephrology, Xiangxi Autonomous Prefecture People’ s Hospital, Jishou, Hunan,416000, China
  • Online:2025-07-31 Published:2025-07-18

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摘要： 目的 探究长链非编码 RNA TONCS_ 00279227 ( Linc279227) 对糖尿病肾病小鼠肾损伤的影响及机制。 方法 小鼠分为 Control 组和模型组, 模型组 db / db 小鼠造模成功后取小鼠肾组织, qRT-PCR 检测小鼠肾组织 Linc279227、 PINK1 和 Parkin mRNA 表达, 蛋白质印迹检测小鼠肾组织自噬相关蛋白微管相关蛋白轻链 3-Ⅱ (microtubule-associated protein light chain 3-Ⅱ , LC3-Ⅱ ) 和 P62 蛋白表达以及 PTEN 诱导假定激酶 1 (PTEN induced putative kinase 1, PINK1) 和 Parkin 蛋白表达。 小鼠肾足细胞 MPC5 细胞分为 Vector组、 Linc27922 组和 Linc27922 + FCCP 组, CCK8 和流式细胞术检测各组细胞增殖凋亡。 蛋白质印迹检测各组细胞 LC3-Ⅱ 、 P62、 PINK1 和 Parkin 蛋白表达。 结果 与 Control 组相比, 模型组小鼠肾组织 Linc279227、P62 的表达显著上调 (P< 0. 01), PINK1 和 Parkin mRNA 和蛋白以及 LC3-Ⅱ 蛋白表达显著下调 (P< 0. 01);与 Vector 组相比, Linc279227 组 MPC5 细胞 PINK1 和 Parkin mRNA 和蛋白以及 LC3-Ⅱ 表达显著下调 ( P< 0. 01), P62 表达显著上调 (P< 0. 01); 与 Linc279227 组相比, Linc27922 + FCCP 组 MPC5 细胞 LC3-Ⅱ 表达上调 (P< 0. 01), P62 显著下调 (P< 0. 01), 细胞增殖能力显著增加 (P< 0. 05), 细胞凋亡显著降低 ( P< 0. 01)。 结论 Linc279227 通过调控 PINK1 / Parkin 通路介导肾足细胞线粒体自噬影响糖尿病肾病小鼠肾损伤。

关键词: 糖尿病肾病, Linc279227, 自噬, PINK1 / Parkin 通路

Abstract: Objective To explore the effect and mechanism of TONCS _ 00279227(Linc279227) on renal injury in diabetes nephropathy mice. Methods Mice were divided into aControl group and a Model group. After successful modeling of db / db mice in the Model group, the mice kidney tissues were taken. qRT-PCR was used to detect the expression levels of Linc279227, PINK1, and Parkin in mice kidney tissues. Western blotting was used to detect the protein expression levels of LC3-Ⅱ , P62, PINK1, and Parkin in mice kidney tissues. Mouse renal podocyte MPC5 cells were divided into 3 groups: Vector group, Linc27922 group, and Linc27922 group. CCK8 and flow cytometry were used to detect cell proliferation and apoptosis. Western blotting was used to detect the expression levels of LC3-Ⅱ , P62, PINK1, and Parkin proteins in eachgroup of cells. Results Compared with those in the Control group, the expression levels of Linc279227 and P62 protein in the renal tissues of the model group mice were significantly upregulated (P< 0. 01), while the expression levels of PINK1 and Parkin mRNA and proteins and the LC3-Ⅱ protein were significantly downregulated (P < 0. 01) . Compared with those in the Vectorgroup, the mRNA and protein expression levels of PINK1 and Parkin and the protein expression level of LC3-Ⅱ in MPC5 cells of the Linc279227 group were significantly downregulated (P < 0. 01), and the expression level of P62 was significantly upregulated (P < 0. 01) . Compared with those inthe Linc279227 group, the LC3-Ⅱ expression level of MPC5 cells in the Linc27922 + FCCP group wasupregulated (P < 0. 01), the expression level of P62 was significantly downregulated (P < 0. 01), the cell proliferation ability was significantly increased (P<0. 05), and the cell apoptosis was significantly reduced (P < 0. 01) . Conclusion Linc279227 can mediate mitochondrial autophagy of nephropodocytes by regulating the PINK1 / Parkin pathway to affect renal injury in diabetes nephropathy mice.

Key words: diabetes nephropathy, Linc279227, autophagy, PINK1 / Parkin pathway

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