Methotrexate (MTX) is a folic acid antagonist, widely used as a chemotherapeutic and immunosuppressive drug, but it is toxic to reproductive systems. In recent years, the era of stem cell applications becomes a promising point as a possible therapeutic agent in male infertility. This study is aimed at evaluating the therapeutic effects of stem cells at histological, molecular, biochemical, and functional levels in a methotrexate-induced testicular damage model. Material and Methods. Thirty rats were divided randomly into three groups (ten rats each): group 1 (control): animals received an intraperitoneal injection of 2 ml phosphate-buffered saline per week for 4 weeks, group 2 (MTX-treated group): animals were intraperitoneally injected with methotrexate (8 mg/kg) once weekly for 4 weeks, and group 3 (ADMSC-treated group): methotrexate-treated animals received a single dose of 1 × 10 6 stem cells/rat at the 5th week. At the 8th week, blood samples were collected for hormonal analysis; then, animals were sacrificed. The testes were dissected; the right testis was stained with hematoxylin and eosin. Random sections were taken from group 3 and examined with a fluorescent microscope. The left testis was divided into two specimens: the first was used for an electron microscope and the second was homogenized for molecular and biochemical assessments. Results. Group 2 showed significant histological changes, decreased free testosterone level, decrease in stem cell factor expression, and dysfunction of the oxidation state. The results revealed significant improvement of these parameters. Conclusion. Transplantation of adipose tissue-derived stem cells (ADMSCs) can improve the testicular damage histologically and functionally in a rat model.

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CAN is one of the major chronic complications of DMII. Clinical investigations have revealed that uncontrolled DM II is frequently associated with lower levels of BDNF. This study assessed whether diminished BDNF level is the reason of CAN caused by DM II and if swimming aerobic exercise can increase BDNF level to ameliorate that CAN in rats. Sixty rats were divided into six groups. Group I; Normal (N), Group 2; BDNF blocker, Group 3; DM II, Group 4; DM II + BDNF, Group 5; DM II + Swimming exercise and Group 6; DM II + Swimming exercise + BDNF blocker. Induction of DM II was done by intraperitoneal injection of 180 mg/kg of Nicotinamide 30 minutes before injection of 50 mg/kg Streptozocin. Swimming exercise began with a 1-week adaptationwith gradual increase of swimming duration until reaching 1h swimming/day at the end of the 1st week. Then, a 7-weeks training program with 5 days/week swimming was followed. The duration of the experiment was 8 weeks during which the following parameters were measured: body weight, random blood glucose "RBG" level, plasma insulin level, heart rate "HR", systolic blood pressure "SBP", heart rate variability "HRV", baroreflex sensitivity "BRS", vascular sympathetic tone "VST" and plasma BDNF. Results revealed that BDNF significantly improved RBG level, HRV, VMT and BRS. Swimming exercise significantly increases plasma BDNF level and also improved CAN. Conclusively, BDNF can be used as a treatment regimen for CAN. Also swimming exercise has great therapeutic effect on CAN maybe by producing BDNF.