Fig. 3

Exercise suppresses the IRE1α-TXNIP/ROS-NLRP3 pathway and improves the phenotype of PCOS rats. Rats received DHEA to induce polycystic ovary syndrome followed by exercise treatment. A Tissues were stained with H&E for revealing ovarian and follicular morphology. B Abdominal adipose tissue were stained with H&E. C Serum LH and FSH levels were analyzed using ELISA. D The expression of AR and CYP11α1 in ovaries was assessed by western blot. E–F The expression of NLRP3 inflammasome activation factors (GSDMD, ASC, IL-1β and IL-18) (E) and fibrosis factors (TGF-β, α-SMA, β-catenin and fibronectin) (F) in ovaries was assessed by qRT-PCR. (G-H) The expression of NLRP3 inflammasome activation factors (GSDMD, GSDMD-C, ASC, IL-1β and IL-18) (G) and fibrosis factors (collagen I, β-catenin, P-SMAD3, α-SMA, TGF-β) (H) in ovaries was assessed by western blot. I Collagen in ovarian slices was revealed by Masson staining. J-K Serum MDA levels (J) and SOD activity (K) were analyzed using an enzymatic colorimetric method. L The expression levels of IRE1α, TXNIP and NLRP3 in ovaries were analyzed by western blot assay. Data are shown as the mean ± SD. *p ≤ 0.05, **p ≤ 0.01. DHEA, dehydroepiandrosterone; D + E, DHEA + Exercise; LH, luteinizing hormone; FSH, follicle stimulating hormone; AR, androgen receptor; CYP11α1, cytochrome p450 11; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; GSDMD, gasdermin D; ASC, apoptosis-associated speck-like protein containing a CARD; IL-1β, interleukin-1β; IL-18, interleukin-18; TGF-β, transforming growth factor-beta; α-SMA, a-smooth muscle actin; GSDMD-C, C-terminal fragment of gasdermin D; MDA, malondialdehyde; SOD, superoxide dismutase; IRE1α, inositol-requiring enzyme 1α; TXNIP, thioredoxin-interacting protein; NLRP3, NOD-like receptor family pyrin domain containing 3