Abstract：Objective:To investigate the effect of LncRNA SNHG16 (long non-coding RNA small nucleolar RNA host gene 16) on high glucose induced cardiomyocyte apoptosis by regulating miR-93-5p (microRNA-93-5p)/TXNIP (thioredoxin interacting protein). Methods: The cell model of diabetes cardiomyopathy was constructed in vitro, and qRT-PCR was used to detect the relative expression levels of LncRNA SNHG16 and miR-93-5p. Cardiomyocyte AC16 was assigned into Control group, Model group, sh-NC group, sh-SNHG16 group, sh-SNHG16+inhibitor NC group, and sh-SNHG16+miR-93-5p inhibitor group, miR-NC group, miR-93-5p mimics group, miR-93-5p mimics+pcDNA group, miR-93-5p mimics+TXNIP group. The relative expression levels of LncRNA SNHG16, miR-93-5p and TXNIP mRNA in AC16 cells of each group were detected by qRT-PCR, the cell proliferation ability was detected by CCK-8 kit method, the cell apoptosis was detected by flow cytometry, the levels of oxidative stress factors were detected by ELISA, and Western blotting was used The expression levels of TXNIP and apoptotic proteins in cells were detected by blot method, and the dual-luciferase reporter gene assay was used to verify the targeting relationship between miR-93-5p and LncRNA SNHG16 and TXNIP. Results: Compared with the Control group, the relative expression levels of LncRNA SNHG16 and TXNIP mRNA, apoptosis rate, protein expression levels of TXNIP, Bax, Caspase 3, Cleaved caspase 3, and level of MDA in AC16 cells in the Model group were greatly higher, the cell viability, expression level of miR-93-5p, protein expression level of Bcl-2, and activity of SOD were greatly lower (P<0.05). Silting the expression of LncRNA SNHG16 or overexpression of miR-93-5p inhibited cell apoptosis and oxidative stress by up-regulating the expression of miR-93-5p (P<0.05). Overexpression of miR-93-5p can improve the pathological changes of high-glucose induced AC16 cells by down-regulating the expression of TXNIP (P<0.05). The dual luciferase reporter gene experiment demonstrated the targeting relationship between miR-93-5p with LncRNA SNHG16 and TXNIP. Conclusion: LncRNA SNHG16 is overexpressed in high glucose induced AC16 cells. Silencing LncRNA SNHG16 can sponge miR-93-5p, downregulate TXNIP expression, inhibit AC16 cell oxidative stress and apoptosis, and enhance its activity.
基金资助:湖北省卫生健康委员会中医药科研项目,(编号:ZY2021M047)
通讯作者:
胡有志
引用本文:
胡艺琼, 余渊, 胡有志. LncRNA SNHG16调节miR-93-5p/TXNIP轴对高糖诱导的心肌细胞凋亡的影响[J]. 河北医学, 2025, 31(8): 1289-1296.
HU Yiqiong, YU Yuan, et al. The Effects of LncRNA SNHG16 Regulating the miR-93-5p/TXNIP Axis on Cardiomyocyte Apoptosis Induced by High Glucose. HeBei Med, 2025, 31(8): 1289-1296.
[1] Wang T,Li N,Yuan L,et al.MALAT1/miR-185-5p mediated high glucose-induced oxidative stress,mitochondrial injury and cardiomyocyte apoptosis via the RhoA/ROCK pathway[J].Cell Mol Med,2023,27(17):2495-2506. [2] Hu Y,Luo M,Xue Y,et al.LncRNA Pvt1 aggravates cardiomyocyte apoptosis via the microRNA-216/Ccnd3 axis[J].Heliyon,2024,10(19):38261-38271. [3] Chu P M,Yu C C,Tsai K L,et al.Regulation of oxidative stress by long non-coding RNAs in vascular complications of diabetes[J].Life (Basel),2022,12(2):274. [4] Liu Y,Zhang M,Zhong H,et al.LncRNA SNHG16 regulates RAS and NF-κB pathway-mediated NLRP3 inflammasome activation to aggravate diabetes nephropathy through stabilizing TLR4[J].Acta Diabetol,2023,60(4):563-577. [5] Gao S,Dong Y,Yan C,et al.The role of exosomes and exosomal microRNA in diabetic cardiomyopathy[J].Front Endocrinol (Lausanne),2024,14(1):1-11. [6] 刘斌,刘娜,曹广林.miR-93-5p对缺氧/复氧H9c2心肌细胞凋亡的作用机制研究[J].中西医结合心脑血管病杂志,2023,21(21):3931-3935. [7] BorowieC A M,Waszczuk A,Olakowska E,et al.TXNIP inhibition in the treatment of diabetes.Verapamil as a novel therapeutic modality in diabetic patients[J].Med Pharm Rep,2022,95(3):243-250. [8] Chen M,Wang R,Liao L,et al.Danshen decoction targets miR-93-5p to provide protection against MI/RI by regulating the TXNIP/NLRP3/Caspase-1 signaling pathway[J].Phytomedicine,2024,135:156225. [9] Shen M,Wu Y,Li L,et al.CircMAP3K5 promotes cardiomyocyte apoptosis in diabetic cardiomyopathy by regulating miR-22-3p/DAPK2 Axis[J].Diabetes,2024,16(1):13471-13481. [10] Huang L,Xiong S,Liu H,et al.Silencing LncRNA SNHG16 suppresses the diabetic inflammatory response by targeting the miR-212-3p/NF-κB signaling pathway[J].Diabetol Metab Syndr,2023,15(1):119-130. [11] 王冰,于欣雨,陈天驰,等.环状RNA-SCAF8通过miR-93-5p/TXNIP通路促进血管内皮细胞焦亡[J].浙江大学学报(医学版),2023,52(4):473-484. [12] Zhao L,Chen H,Wu L,et al.LncRNA KCNQ1OT1 promotes the development of diabetic nephropathy by regulating miR-93-5p/ROCK2 axis[J].Diabetol Metab Syndr,2021,13(1):108-120. [13] Choi EH,Park S J.Txnip.A key protein in the cellular stress response pathway and a potential therapeutic target[J].Exp Mol Med,2023,55(7):1348-1356. [14] Zhang Y,Li B,Fu Y,et al.Txnip promotes autophagic apoptosis in diabetic cardiomyopathy by upregulating FoxO1 and its acetylation[J].Cell Signal,2024(124):111469.
2025, Vol. 31 
冀公网安备13080202000786号