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©The Author(s) 2024.
World J Diabetes. Jan 15, 2024; 15(1): 105-125
Published online Jan 15, 2024. doi: 10.4239/wjd.v15.i1.105
Published online Jan 15, 2024. doi: 10.4239/wjd.v15.i1.105
Figure 8 Myricetin regulated the polarization of RAW 264.
7 cells through the PI3K/Akt signaling pathway in diabetic nephropathy mice. A-D: CD86-labeled and CD206-labeled RAW 264.7 macrophages under the 33.3 mmol/L glucose condition and after 25 μM myricetin treatment and LY294002 administration assessed by flow cytometry (A) and for protein levels of inducible nitric oxide synthase (iNOS), arginase-1 (Arg-1), phosphorylated-Akt (at S473) and Akt by western blotting (B) or mRNA levels of iNOS, tumor necrosis factor-alpha, interleukin (IL)-6, IL-1β, IL-10, and Arg-1 by reverse transcription PCR (C), and for secreted levels of TNF-α,IL-6, IL-1β, and IL-10 by ELISA. Arg-1: Arginase-1; TNF-α: Tumor necrosis factor-alpha; IL: Interleukin; iNOS: Inducible nitric oxide synthase; HG: High-glucose. bP < 0.05.
- Citation: Xu WL, Zhou PP, Yu X, Tian T, Bao JJ, Ni CR, Zha M, Wu X, Yu JY. Myricetin induces M2 macrophage polarization to alleviate renal tubulointerstitial fibrosis in diabetic nephropathy via PI3K/Akt pathway. World J Diabetes 2024; 15(1): 105-125
- URL: https://www.wjgnet.com/1948-9358/full/v15/i1/105.htm
- DOI: https://dx.doi.org/10.4239/wjd.v15.i1.105