Cordyceps cicadae polysaccharides attenuate diabetic nephropathy via the miR‐30a‐3p/TRIM16 axis

Abstract Objective The molecular mechanism of the protective effect of Cordyceps cicadae polysaccharides (CCPs) on renal tubulointerstitial fibrosis in diabetic nephropathy (DN) is still unclear. This study aims to further understand the molecular mechanisms behind the therapeutic benefits of CCP on diabetic nephropathy. Methods Mice were randomly assigned into six groups (n = 8). Cordyceps cicadae polysaccharide dissolved in 5% dimethyl sulfoxide was administered by gavage for 12 consecutive weeks. The CCP doses were divided into low, medium, and high, 75, 150, and 300 mg/kg/day, respectively. The efficacy of CCP was determined by assessing the renal function and histological alterations in diabetic db/db mice. The degree of glomerular mesangial dilatation and sclerosis was evaluated using semiquantitative markers. Cell viability, apoptosis, epithelial–mesenchymal transition (EMT), inflammation, oxidative stress, and mitochondrial reactive oxygen species (ROS) in high glucose (HG)‐cultured MPC5 podocytes were determined. The interaction of miR‐30a‐3p and tripartite motif‐containing protein 16 (TRIM16) was examined by luciferase reporter assay. Western blotting, reverse transcription‐polymerase chain reaction, and immunofluorescence were used to analyze gene and protein expressions. Results The in vivo findings illustrated that CCP may protect mice with type 2 diabetes from inflammation and oxidative damage (P