Fig 2: Detection of inflammation and oxidative-reduction related factors in heart tissue of mice using ELISA method (A) iNOS, (B) COX-2, (C) CCL9, (D) CXCL1, (E) CXCL9 and (F) CXCL11 in mouse heart tissues. Data are presented as the mean ± SD. Each experiment was repeated three times independently. *P<0.05 vs. NC group. #P<0.05 vs. OT group. DHE, dehydrocostus lactone; TXNIP, thioredoxin-interacting protein; NC, negative control; OT, DHE treatment group; OI, DHE treatment combined with TXNIP inhibition group; OH, DHE treatment combined with TXNIP overexpression group; iNOS, inducible nitric oxide synthase; COX-2, cyclooxygenase-2; CCL9, C-C motif ligand 9; CXCL, chemokine C-X-C motif ligand.

Fig 3: Overview of obesity and radiation associated adipose dysfunction promotes a pro-tumorigenic prostate microenvironment. This stress-adapted phenotype is characterized by enhanced survival signaling, oxidative stress, chronic inflammation, senescence-associated remodeling, and ECM remodeling, collectively establishing a tumor-permissive stromal niche. The obese and irradiated obese adipose microenvironment differentiates prostate fibroblasts toward myofibroblasts and senescent fibroblasts. In turn, myofibroblasts or senescent fibroblasts under obese and irradiated obese adipose microenvironments secrete pro-inflammatory chemokines, including CXCL10 and CXCL11, which promote prostate cancer migration through CXCR3-mediated paracrine signaling. Radiation exposure sustains obesity-associated pathological state within the prostate microenvironment and prostate fibroblasts.