Myricetin induces M2 macrophage polarization to alleviate renal tubulointerstitial fibrosis in diabetic nephropathy via PI3K/Akt pathway

Figure 3 Myricetin inhibited inflammation factors and fibrosis in the renal tissue of diabetic nephropathy mice. A: Immunofluorescent staining of F4/80 protein; B: Tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, IL-1β, and IL-10 mRNA levels; C: Serum TNF-α, IL-6, IL-1β, and IL-10 Levels; D: Immunofluorescent staining of collagen-1a1 (Col1a1) protein; E: Reverse transcription-PCR analysis of Col1a1 and alpha-smooth muscle actin (α-SMA) mRNAs; F: Western blotting analysis of Col1a1 and α-SMA proteins; G: Masson’s trichrome staining (left) and renal fibrosis analysis (right); H: Sirius-red staining (left) and fibrosis analysis (right). TNF-α: Tumor necrosis factor-alpha; α-SMA: Alpha-smooth muscle actin; IL: Interleukin; Col1a1: Collagen-1a1. ^bP < 0.05.