敲低PIAS3缓解血糖波动诱导的大鼠心肌细胞系H9c2氧化应激及线粒体功能障碍

doi:10.16352/j.issn.1001-6325.2025.12.1593

基础医学与临床 ›› 2025, Vol. 45 ›› Issue (12): 1593-1599.doi: 10.16352/j.issn.1001-6325.2025.12.1593

敲低PIAS3缓解血糖波动诱导的大鼠心肌细胞系H9c2氧化应激及线粒体功能障碍

成永霞¹, 于龙², 李化敏³, 赵硕¹, 张怡扬¹, 刘贵波^4*

1.牡丹江医科大学第一临床医学院病理教研室,黑龙江牡丹江 157011;
2.牡丹江医科大学附属红旗医院儿科,黑龙江牡丹江 157011;
3.牡丹江医科大学附属红旗医院病理科,黑龙江牡丹江 157011;
4.牡丹江医科大学基础医学院解剖教研室,黑龙江牡丹江 157011

收稿日期:2025-04-30 修回日期:2025-06-23 出版日期:2025-12-05 发布日期:2025-11-25
通讯作者: ^*lgb20073@163.com
基金资助:
黑龙江省医药卫生科研课题(20220101040735);黑龙江省省属高等学校基本科研业务费攀登项目(2022-KYYWFMY-0002)

Knockdown of PIAS3 alleviates glucose fluctuation-induced oxidative stress and mitochondrial dysfunction in rat cardiomyocyte cell line H9c2

CHENG Yongxia¹, YU Long², LI Huamin³, ZHAO Shuo¹, ZHANG Yiyang¹, LIU Guibo^4*

1. Department of Pathology, the First Clinical Medical College, Mudanjiang Medical University, Mudanjiang 157011;
2. Pediatrics Department, Hongqi Hospital Affiliated to Mudanjiang Medical University, Mudanjiang 157011;
3. Pathology Department, Hongqi Hospital Affiliated to Mudanjiang Medical University, Mudanjiang 157011;
4. Department of Anatomy, Basic Medical College, Mudanjiang Medical University, Mudanjiang 157011, China

Received:2025-04-30 Revised:2025-06-23 Online:2025-12-05 Published:2025-11-25
Contact: ^*lgb20073@163.com

摘要/Abstract

摘要： 目的探讨活化STAT抑制蛋白3(PIAS3)对血糖波动诱导的大鼠心肌细胞氧化应激、线粒体功能障碍的影响。方法体外培养大鼠心肌细胞系H9c2,实验分为正常糖对照组(Control组)、渗透压对照组(MG组)、高糖组(HG组)、波动性高血糖组(IHG组)、波动性高血糖+NC对照组(IHG+siRNA NC组)和波动性高血糖+PIAS3敲低组(IHG+PIAS3 siRNA组)。CCK-8检测细胞增殖,试剂盒检测LDH释放量、MDA、GSH含量和SOD活力;JC-1染色结合流式检测线粒体膜电位,DCFH-DA及MitoSOX染色分别检测细胞及线粒体ROS含量;Western blot检测PI3K、p-PI3K、AKT和p-AKT蛋白表达。结果与对照组比较,波动性高血糖可促进氧化应激及线粒体功能障碍,PIAS3的表达显著上调(P＜0.001),p-PI3K、p-AKT蛋白水平显著下调(P＜0.001);敲低PIAS3显著缓解血糖波动诱导的氧化应激及线粒体功能损伤,p-PI3K、p-AKT蛋白水平显著升高(P＜0.001)。结论敲低PIAS3可能通过激活PI3K/AKT信号通路缓解血糖波动诱导的大鼠心肌细胞系氧化应激及线粒体功能障碍。

关键词: PIAS3, 血糖波动, 氧化应激, 线粒体功能障碍

Abstract: Objective To investigate the effect of PIAS3 on glucose fluctuation-induced oxidative stress and mitochondrial dysfunction in rat cardiomyocytes. Methods H9c2 were cultured in vitro, and divided into normal glucose control group(Control), mannitol-induced osmotic pressure control group(MG), constant high glucose group(HG), intermittent hyperglycemia group(IHG), IHG+siRNA NC group, and IHG+PIAS3 siRNA group. Cell proliferation was assessed using CCK-8 assay. LDH release,MDA and GSH levels, as well as SOD activity, were detected using corresponding kits. Mitochondrial membrane potential was evaluated via JC-1 staining combined with flow cytometry. ROS levels in cells and mitochondria were determined using DCFH-DA and MitoSOX staining, respectively. Protein expression of PI3K, p-PI3K, AKT, and p-AKT was analyzed by Western blot. Results Compared with the control group, intermittent hyperglycemia promoted oxidative stress and mitochondrial dysfunction, significantly upregulated PIAS3 expression(P＜0.001) and downregulated p-PI3K and p-AKT protein levels(P＜0.001). Knockdown of PIAS3 significantly alleviated oxidative stress and mitochondrial dysfunction induced by glucose fluctuations, and increased p-PI3K and p-AKT protein levels(P＜0.001). Conclusions Knockdown of PIAS3 may alleviate glucose fluctuation-induced oxidative stress and mitochondrial dysfunction in ratcardiomyocytes by activating the PI3K/AKT signaling pathway.

Key words: PIAS3, glucose fluctuation, oxidative stress, mitochondrial dysfunction

中图分类号:

R692
R587.2

成永霞, 于龙, 李化敏, 赵硕, 张怡扬, 刘贵波. 敲低PIAS3缓解血糖波动诱导的大鼠心肌细胞系H9c2氧化应激及线粒体功能障碍[J]. 基础医学与临床, 2025, 45(12): 1593-1599.

CHENG Yongxia, YU Long, LI Huamin, ZHAO Shuo, ZHANG Yiyang, LIU Guibo. Knockdown of PIAS3 alleviates glucose fluctuation-induced oxidative stress and mitochondrial dysfunction in rat cardiomyocyte cell line H9c2[J]. Basic & Clinical Medicine, 2025, 45(12): 1593-1599.

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敲低PIAS3缓解血糖波动诱导的大鼠心肌细胞系H9c2氧化应激及线粒体功能障碍

Knockdown of PIAS3 alleviates glucose fluctuation-induced oxidative stress and mitochondrial dysfunction in rat cardiomyocyte cell line H9c2

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