Fig. 3From: Suppression of p66Shc prevents hyperandrogenism-induced ovarian oxidative stress and fibrosisResveratrol inhibits p66Shc phosphorylation and fibrotic factors activation in rat ovaries. Rats received DHEA for the induction of polycystic ovarian syndrome, together with or without resveratrol treatment. a Sirt1, α-SMA, collagen I A1, CTGF, and p-p66Shc expression in rat ovaries (60×) was analyzed by double immunofluorescence staining. Images are representative of three independent experiments with similar results. b The expression of fibrotic factors and p-p66Shc in ovaries was assessed by western blot. The panel on the right shows the quantitative analysis. c The mRNA levels of AR was analyzed by real-time PCR. d Relative expression of p66Shc and fibrotic factors in rat ovaries was determined by real-time PCR. n = 7 in each group. Three independent experiments were performed with similar results. Data are shown as mean ± SD & mean ± SEM. *p ≤ 0.05, **p ≤ 0.01 vs. Blank; #p ≤ 0.05, ##p ≤ 0.01 vs. DHEA treatment. DHEA dehydroepiandrosterone, AR androgen receptor, CTGF connective tissue growth factor, Sirt1 sirtuin 1, p-p66Shc phosphorylated 66-kDa Src homology 2 domain-containing proteinBack to article page