Journal: The FASEB Journal

Article Title: Aberrant DNMTs Promote TXNIP Upregulation and Ovarian Fibrosis in PCOS

doi: 10.1096/fj.202505030R

Figure Lengend Snippet: 5‐Aza treatment inhibits TXNIP and ovarian fibrosis in PCOS‐like rats. Rats received DHEA in the presence or absence of 5‐Aza treatment ( n = 8 in each group). (A) Ovarian and follicular morphology was assessed using H&E staining. (B) TXNIP expression in ovaries was analyzed using immunohistochemical staining. (C) Protein levels of DNMTs and TXNIP in two representative ovaries of each group were assessed using western blot (left panel). Band intensities were quantified ( n = 3; right panel). (D) Protein levels of pro‐fibrotic factors (collagen I, β ‐catenin, P‐SMAD3, α ‐SMA, and TGF‐ β ) in two representative ovaries of each group were assessed using western blot (left panel). Band intensities were quantified ( n = 3; right panel). Data are shown as the mean ± SD. * p ≤ 0.05, ** p ≤ 0.01. Each treatment group was compared with the control group. DHEA, dehydroepiandrosterone; DNMT1, DNA methyltransferase 1; DNMT3A, DNA methyltransferase 3A; DNMT3B, DNA methyltransferase 3B; TXNIP, thioredoxin‐interacting protein.

Article Snippet: To establish an in vitro hyperandrogenic PCOS‐like model, cells were treated with various concentrations (0.5, 2, and 5 μM) of dihydrotestosterone (DHT; Meilun Biological Technology Corporation, China) for 48 h. For determining the regulation of TXNIP, 5‐Aza (10 μM; MCE) or flutamide (20, 50 μM; Selleck, China) was added 24 h after the initiation of DHT treatment.

Techniques: Staining, Expressing, Immunohistochemical staining, Western Blot, Control

Journal: The FASEB Journal

Article Title: Aberrant DNMTs Promote TXNIP Upregulation and Ovarian Fibrosis in PCOS

doi: 10.1096/fj.202505030R

Figure Lengend Snippet: 5‐Aza treatment inhibits hyperandrogenism‐induced upregulation of TXNIP and pro‐fibrotic factors in GCs. Primary GCs were treated with DHT followed by 5‐Aza and MG132 ( n = 3 in each group). (A) Protein levels of DNMTs and TXNIP in GCs were assessed using western blot (left panel). Band intensities were quantified ( n = 3; right panel). (B‐D) Levels of DNMT1, DNMT3A, and TXNIP in GCs were analyzed using immunofluorescence staining (60×) (left panel). Fluorescence intensities were quantified ( n = 3; right panel). (E) Protein levels of pro‐fibrotic factors (collagen I, β ‐catenin, P‐SMAD3, α ‐SMA, and TGF‐ β ) in GCs were assessed using western blot. (F) Band intensities were quantified (E) ( n = 3). (G) Protein levels of TXNIP in GCs were assessed using western blot (upper panel). Band intensities were quantified ( n = 3; lower panel). Data are shown as the mean ± SD. * p ≤ 0.05, ** p ≤ 0.01. Each treatment group was compared with the control group. DHT, dihydrotestosterone; DNMT1, DNA methyltransferase 1; DNMT3A, DNA methyltransferase 3A; DNMT3B, DNA methyltransferase 3B; N.S, not significant; TXNIP, thioredoxin‐interacting protein.

Article Snippet: To establish an in vitro hyperandrogenic PCOS‐like model, cells were treated with various concentrations (0.5, 2, and 5 μM) of dihydrotestosterone (DHT; Meilun Biological Technology Corporation, China) for 48 h. For determining the regulation of TXNIP, 5‐Aza (10 μM; MCE) or flutamide (20, 50 μM; Selleck, China) was added 24 h after the initiation of DHT treatment.

Techniques: Western Blot, Immunofluorescence, Staining, Fluorescence, Control