LncRNA SNHG16调节miR-93-5p/TXNIP轴对高糖诱导的心肌细胞凋亡的影响

doi:10.3969/j.issn.1006-6233.2025.08.010

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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.

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	HU Yiqiong
	YU Yuan
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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[J]. HeBei Med, 2025, 31(8): 1289-1296.

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http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2025.08.010 OR http://www.hbyxzzs.cn/EN/Y2025/V31/I8/1289

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