Rosiglitazone attenuates high glucose-induced proliferation, inflammation, oxidative stress and extracellular matrix accumulation in mouse mesangial cells through the Gm26917/miR-185-5p pathway

Abstract

Rosiglitazone (RSG) is widely used to reduce the amount of sugar in the blood of patients with diabetes mellitus. Diabetic nephropathy is the most common microvascular complication of diabetes. The role of RSG in diabetic nephropathy is not fully understood. Diabetic nephropathy model was constructed in high glucose (HG)-treated mouse mesangial cells. The effects of RSG on cell viability and cell cycle were investigated using cell counting kit-8 (CCK-8) assay and flow cytometry assay. Oxidative stress was assessed according to ROS production and SOD activity in cells. Inflammatory responses were assessed according to the releases of inflammatory cytokines. Extracellular matrix (ECM) accumulation was determined by the levels of fibronectin and collagen IV using western blot. The expression of Gm26917 and microRNA-185-5p (miR-185-5p) was detected by quantitative real-time polymerase chain reaction (qPCR). The interaction between Gm26917 and miR-185-5p was validated by dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and pull-down assay. RSG significantly inhibited HG-induced proliferation, oxidative stress, inflammatory responses and ECM accumulation in mouse mesangial cells. The expression of Gm26917 was induced by HG but weakened by RSG. Gm26917 knockdown alleviated HG-induced proliferation, oxidative stress, inflammatory responses and ECM accumulation in mouse mesangial cells, and Gm26917 overexpression partly abolished the effects of RSG. Moreover, miR-185-5p was a target of Gm26917, and miR-185-5p inhibition recovered proliferation, oxidative stress, inflammatory responses and ECM accumulation in mouse mesangial cells that were alleviated by Gm26917 knockdown. RSG ameliorated HG-induced mouse mesangial cell proliferation, oxidative stress, inflammation and ECM accumulation partially by governing the Gm26917/miR-185-5p pathway.

Down-Regulated miR-130a/b Attenuates Rhabdomyosarcoma Proliferation via PPARG

“…In addition, as a PPARG agonist, rosiglitazone maleate significantly inhibits biological functions in RD cells. Rosiglitazone maleate has traditionally been widely used to reduce sugar in the blood of patients with diabetes mellitus (Zhao et al, 2021). However, investigators have recently demonstrated that rosiglitazone maleate also has a therapeutic effect on various cancers, including lung cancer, breast cancer, and pancreatic cancer (Dang et al, 2018;Wang et al, 2020;Wu et al, 2020;Wang et al, 2021;Zhou et al, 2021).…”

Antioxidant Efficacy of Esculetin against Tert-Butyl Hydroperoxide-Induced Oxidative Stress in HEK293 Cells

“…It also causes glomerular podocyte loss [ 8 ] and endoplasmic reticulum (ER) stress injury to human renal glomerular endothelial cells [ 9 ], both of which contribute to kidney dysfunction. In addition, one study found that oxidative stress increases the proliferation of mesangial cells [ 10 ] and is linked to glomerulonephritis [ 11 ].…”

Rosiglitazone alleviates LPS-induced endometritis via suppression of TLR4-mediated NF-κB activation

“…Studies have shown that RGZ has both insulin-sensitizing effects and anti-in ammatory and immune-modulating effects. RGZ plays its anti-in ammatory roles in the acute and chronic in ammatory responses of many organs such as the heart, lung, kidney, and gastrointestinal tract [11][12][13][14]. Bo et al reported that RGZ pretreatment alleviated LPS-induced placental in ammation and reduced embryonic mortality in mice [15].…”