LncRNA SNHG16靶向miR-425-5p对类风湿关节炎滑膜成纤维细胞增殖和凋亡的影响

Effects of LncRNA SNHG16 Targeting miR-425-5p on the Proliferation and Apoptosis of Synovial Fibroblasts in Rheumatoid Arthritis

该文旨在探究长链非编码RNA(Lnc RNA)SNHG16靶向mi R-425-5p对类风湿关节炎(rheumatoid arthritis,RA)滑膜成纤维细胞增殖和凋亡的影响及其作用机制。通过q RT-PCR检测SNHG16和mi R-425-5p的相对表达量;CCK8、流式细胞术和Western blot分别检测细胞增殖、凋亡及Ki67、Bax蛋白表达情况;双荧光素酶实验检验SNHG16和mi R-425-5p的靶向关系。SNHG16在RA滑膜组织和RA滑膜成纤维细胞中的相对表达量显著增加(P<0.05),miR-425-5p相对表达量显著降低(P<0.05);沉默SNHG16或过表达mi R-425-5p可以明显抑制RA滑膜成纤维细胞的增殖(P<0.05),并促进细胞凋亡(P<0.05)。SNHG16可以靶向调控mi R-425-5p的表达,抑制mi R-425-5p可以部分回复沉默SNHG16对RA滑膜成纤维细胞增殖和凋亡的作用(P<0.05)。SNHG16可以通过上调mi R-425-5p的表达抑制滑膜成纤维细胞的增殖,并诱导其细胞凋亡,为研发治疗和诊断类风湿关节炎的新靶点提供参考数据。

This paper aimed to explore the effect of LncRNA(long non-coding RNA)SNHG16 on the proliferation and apoptosis of RA(rheumatoid arthritis)synovial fibroblasts by targeting miR-425-5p and its mechanism.The relative expression levels of SNHG16 and miR-425-5p were detected by qRT-PCR.Cell proliferation,apoptosis and the expression of Ki67 and Bax proteins were detected by CCK8,flow cytometry and Western blot,respectively.Double luciferase experiment was used to examine the targeting relationship between SNHG16 and miR-425-5p.The relative expression of SNHG16 in RA synovial tissues and RA synovial fibroblasts was significantly increased(P<0.05),and the relative expression of miR-425-5p was significantly decreased(P<0.05).Silencing SNHG16 or overexpression of miR-425-5p significantly inhibited proliferation of RA synovial fibroblasts and promoted cell apoptosis(P<0.05).SNHG16 can target and regulate the expression of miR-425-5p,and inhibiting miR-425-5p can partially restore the effects of silencing SNHG16 on the proliferation and apoptosis of RA synovial fibroblasts(P<0.05).SNHG16 can inhibit the proliferation of synovial fibroblasts by up-regulating the expression of miR-425-5p,and induce their apoptosis,providing reference data for the development of new targets for the treatment and diagnosis of RA.