Protective effect of granulocyte colony stimulating factor on cyclophosphamide-induced prostate injury in rats.

Cyclophosphamide (CPA) is a commonly used chemotherapeutic agent whose metabolites readily accumulate in male reproductive organs such as the testes and epididymis, exhibiting reproductive toxicity. Granulocyte colony-stimulating factor (G-CSF) possesses anti-inflammatory and antioxidant effects, but its protective mechanism against CPA-induced prostate injury remains unclear. This study aimed to investigate the protective effect of G-CSF against CPA-induced prostate injury in rats. Thirty SPF male Sprague-Dawley (SD) rats were randomly divided into a control group (C group), a CPA model group (M group), and a CPA+G-CSF group (G-CSF group). The M and G-CSF groups received intraperitoneal injections of cyclophosphamide (30 mg/kg/d) for 5 consecutive days, while the C group received an equal volume of saline. Starting on the first day after the model was established, the G-CSF group began receiving G-CSF solution via subcutaneous injection at a dose of 50 μg/kg body weight, three times a week for 5 consecutive weeks. Groups C and M received equivalent volumes of saline via subcutaneous injection. Serum and dorsal prostate tissue were collected for analysis after the final dose. Results: Rats in Group M exhibited reduced body weight, prostate weight, citric acid (CA) content, and acid phosphatase (ACP) activity. Hematoxylin and eosin (HE) staining revealed papillary hyperplasia with leukocyte infiltration. Elevated levels of interleukin-1β (IL-1β), IL-18, and C-reactive protein (CRP) increased, malondialdehyde (MDA) levels rose, superoxide dismutase (SOD) decreased, ZnT9 expression declined, and NF-κB nuclear translocation increased. G-CSF significantly reversed these pathological alterations. G-CSF alleviates CPA-induced prostate injury by improving zinc homeostasis through ZnT9 upregulation and suppressing NF-κB-mediated inflammation and oxidative stress, offering a novel therapeutic strategy for its prevention and treatment.