Department of Nephrology, The Affiliated Xuzhou Municipal Hospital of Xuzhou Medical University, First People's Hospital of Xuzhou, Xuzhou, China.
Department of Emergency, The Affiliated Xuzhou Municipal Hospital of Xuzhou Medical University, First People's Hospital of Xuzhou, Xuzhou, China.
Horm Metab Res. 2021 Dec;53(12):818-824. doi: 10.1055/a-1678-6556. Epub 2021 Dec 10.
The study explored the diagnostic value of SNHG5 in diabetic nephropathy (DN) and investigated the role and mechanism on DN via establishing the in vitro HK2 cell model. This study recruited 62 types 2 diabetes mellitus (T2DM) patients, 58 DN patients and 60 healthy controls (HC). The expressions of serum SNHG5 and miR-26a-5p were measured by RT-qPCR analysis. The diagnostic value of SNHG5 in DN was assessed by ROC curve. The in vitro cell model was built to estimate the effects of SNHG5 on cell viability, cell apoptosis, inflammation response and oxidative stress. Serum SNHG5 was increased in DN patients (relative expression: 2.04±0.34) and had the diagnostic value in DN. After HK2 cells were treated with high glucose, the cell viability decreased and apoptosis increased, and the production of inflammatory cytokines and ROS enhanced significantly. It was noticed that inhibition of SNHG5 could reverse the above phenomenon caused by high glucose. Besides, serum miR-26a-5p was diminished in DN patients, and luciferase reporter gene revealed that miR-26a-5p is direct target of SNHG5. These results indicated that inhibition of SNHG5 may mitigate HG-induced renal tubular damage via targeting miR-26a-5p, which providing a new insight into the mechanism of renal tubule damage in DN patients.
本研究通过建立体外 HK2 细胞模型,探讨 SNHG5 在糖尿病肾病(DN)中的诊断价值,并研究其对 DN 的作用及机制。本研究纳入 62 例 2 型糖尿病(T2DM)患者、58 例 DN 患者和 60 例健康对照者(HC)。采用 RT-qPCR 分析检测血清 SNHG5 和 miR-26a-5p 的表达。通过 ROC 曲线评估 SNHG5 在 DN 中的诊断价值。建立体外细胞模型,评估 SNHG5 对细胞活力、细胞凋亡、炎症反应和氧化应激的影响。DN 患者血清 SNHG5 升高(相对表达量:2.04±0.34),具有诊断 DN 的价值。高糖处理 HK2 细胞后,细胞活力下降,凋亡增加,炎症细胞因子和 ROS 产生显著增强。抑制 SNHG5 可逆转高糖引起的上述现象。此外,DN 患者血清 miR-26a-5p 减少,荧光素酶报告基因表明 miR-26a-5p 是 SNHG5 的直接靶标。这些结果表明,抑制 SNHG5 可能通过靶向 miR-26a-5p 减轻 HG 诱导的肾小管损伤,为 DN 患者肾小管损伤的机制提供了新的见解。