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Testosterone plays an important role in maintaining both physical and mental function. Age‐related testosterone depletion contributes to the development of angina, arteriosclerosis, obesity, metabolic syndrome, dementia, frailty, and a range of other conditions. A condition involving age‐related testosterone depletion and the associated clinical symptoms is defined as late‐onset hypogonadism (LOH). LOH is treated by testosterone replacement therapy. Indications for testosterone replacement therapy are determined by evaluating symptoms and signs.

Introduction and Objectives Evidence-based treatment for chronic prostatitis (CP) has not been established so far. Innovative therapy for CP is needed to establish evidence-based therapy. Indoleamine 2,3-dioxygenase1 (IDO1) catalyzes the first and rate-limiting step of tryptophan catabolism through the kynurenine pathway. IDO1 expression in prostate is higher than that of other organs. IDO1 is induced in various tissues during inflammatory disease. Furthermore, protective effect of IDO1 inhibition for inflammation was indicated in some reports. We hypothesize that IDO1 plays a central role for immunological reaction in CP. We investigated the relevance between IDO1 inhibition and CP using autoimmune induced CP model mice. This study was approved by the safety committee for DNA experiments and the animal research committee of our facility (Approval No.18-07 and 20-89). Materials and Methods Ten to twelve weeks old, IDO1 knock out (IDO1 KO) mice were used through the research. Same conditional wild type (WT) mice were set as control. Prostate gland extracted from Wister rat were used as prostate antigen (Pag) for mice. PAg 100µg / 100µl were injected into mice subcutaneously. After creating autoimmune induced CP model mice, inflammatory change in the prostate was investigated using histological, biochemical and immunohistochemical analysis. Results Histological analysis showed suppressive effect of inflammatory cells infiltration and interstitial fibrosis were observed in IDO1 KO CP model mice compared with that of WT CP model mice. Proteomic analysis showed decreased effect of lymphocyte and monocyte related cytokines (CCL2, CCL3) and fibrosis related cytokine (TIMP-1) in IDO1 KO CP model mice compared with that of WT CP model mice. Same results were obtained from immunohistochemical analysis using immunofluorescent stain. Conclusions IDO1 is involved in chronic inflammation via cytokines/chemokines in the prostate. IDO1 inhibition contribute to suppressive effect of chronic inflammation and fibrosis in the prostate. Therefore, IDO1 inhibition might be a novel target therapy for chronic prostatitis. Disclosure Work supported by industry: no.

Introduction & Objectives Testicular ischemia represented by torsion needs emergency surgery to reperfuse testicular blood flow. However, spermatic dysfunction is often led despite appropriate treatment. Pathology of spermatic dysfunction following testicular ischemia-reperfusion injury (IRI) is still unclear. In previous research, Inflammation and excessive oxidative stress were thought to be involved in tissue dysfunction following IRI. We hypothesized that inflammation and excessive oxidative stress plays key role in spermatic dysfunction following testicular IRI. We investigated relevance between Inflammation / excessive oxidative stress and spermatic dysfunction using testicular IRI model mice. Materials & Methods Ten to fifteen weeks old, C57BL/6 male were used through the study. Unilateral (left side) testicular vessels were clamped and de-clamped 1 hour later. Testicular blood flow was resumed. Sham operation mice were set as control. Bilateral testes were removed at 0(during ischemia), 1, 3, 5 weeks after modeling testicular IRI mice. Inflammation and oxidative stress changes in bilateral testis were investigated using histological, biochemical and immunohistochemical analysis. Spermatic changes extracted from the epididymal cauda were investigated using computer aided sperm analysis (CASA). Results Histological analysis using HE and Masson-Trichrome (MT) stain showed invasion of inflammatory cells and destruction of tissue structure from week 1. Inflammatory analysis using comprehensive protein assay and immunofluorescent stain showed increased expression of cytokines (IL-2, IL-3, IL-17A, IL-23), chemokines (CCL2, CCL5, CXCL1, CX3CL1), testes were showed from week1. Oxidative stress and cell death analysis using representative candidates (8-OHdG, ROS) showed increased expression of representative candidates from week0. Spermatic analysis showed that obvious decreased spermatic concentration and motility were showed from week 1. In contralateral testes, slow decreased spermatic concentration and motility was showed from week 1. Conclusions Spermatic dysfunction following testicular-ischemia reperfusion injury was induced in inflammatory and excessive oxidative stress changes. Inflammatory and excessive oxidative stress changes might be a novel regulatory factor for spermatic dysfunction following testicular ischemia-reperfusion injury. Disclosure Work supported by industry: no.