Berberine Alleviates Oxidative Stress in Islets of Diabetic Mice by Inhibiting miR-106b Expression and Up-Regulating SIRT1.

Mounting studies have indicated the role of berberine, SIRT1, and oxidative stress in diabetes, respectively. However, few studies have demonstrated their correlation and regulation function in diabetes. Therefore, the protective effect of berberine in diabetic and the underlying core mechanism were investigated in the current study. Diabetic mice model in vivo were established. Mouse pancreatic beta-cell line NIT-1 cells were treated with 30 mM high glucose to induce diabetic condition in vitro. Serum biochemical parameters (glucose, total cholesterol, and triglycerides) were detected. Oxidative stress indicators (MDA, SOD1), along with miR-106b and SIRT1 expression in islets and cells were also assessed. Direct targeting relationship between miR-106b and SIRT1 was discussed by dual luciferase reporter gene assay. Diabetic model in vivo and in vitro were both established successfully. The expression of serum biochemical parameters was increased, and oxidative stress parameters, and miR-106b, SIRT1 were abnormally expressed in diabetic mice and NIT-1 cells. Meanwhile, berberine could alleviate oxidative stress injury in diabetic progression. Through dual luciferase reporter gene assay, we found that SIRT1 was a target gene of miR-106b. In addition, miR-106b over-expression could reverse the protection of berberine in NIT-1 cells against from oxidative stress induced by high glucose. Berberine could attenuate oxidative stress of diabetic mice at least partly through miR-106b/SIRT1 pathway and affecting the function of islets, which might be beneficial in reducing the cardiovascular risk factors in diabetes. J. Cell. Biochem. 118: 4349-4357, 2017. © 2017 Wiley Periodicals, Inc.

Shikonin Inhibits Inflammatory Response in Rheumatoid Arthritis Synovial Fibroblasts via lncRNA-NR024118.

Background. Shikonin is a major chemical component of zicao that possesses anti-inflammatory properties and the ability to mediate cellular and humoral immunity, especially in rheumatoid arthritis (RA). We investigated the impact of shikonin on inflammatory response in RA synovial fibroblasts using the CAIA model. Methods. Severe polyarticular arthritis was induced in Balb/c female mice. Expressions of lncRNA-NR024118, SOCS3, proinflammatory cytokines, and MMPs were evaluated using RT-RCR. Histone acetylation and SOCS3 protein expression were assessed by ChIP assay and western blot, respectively. Results. Mice treated with shikonin showed an abrogation of soft tissue and bone lesions. Shikonin remarkably enhanced the expression of NR024118 and SOCS3 and suppressed the secretion and expression of IL-6, IL-8, and MMPs. Proliferation of cultured RA synovial fibroblasts in the presence of IL-1ß was also significantly inhibited by shikonin. Moreover, shikonin dose-dependently increased acetylation of histone H3 at the promoter of NR024118. Finally, NR024118 overexpression and interference significantly changed SOCS3 expression and NR024118 interference could reverse regulation of shikonin on SOCS3, proinflammatory cytokines, and MMPs expression level in MH7A cells. Conclusion. Our results reveal that, in the CAIA mouse model of RA, shikonin has disease modifying activity that is attributable to the inhibition of inflammatory response via lncRNA-NR024118.