This study aimed to investigate the effect of naringenin (Nar) on cadmium (Cd)-induced testicular toxicity. Twenty-four male Sprague–Dawley (SD) rats aged 5 weeks were used. Rats were administered with 0.9% NaCl (control group), CdCl₂ (2 mg/kg b.w. intraperitoneally), Nar (50 mg/kg b.w, orally), and CdCl₂ + Nar (2 mg/kg b.w intraperitoneally and 50 mg/kg b.w. orally, respectively) for 4 weeks. Results showed that body weight, relative testis weights, and sperm quality decreased in the Cd-treated group, and Cd accumulated in serum and testes. Pathological examination showed that Cd can cause testicular damage. Cd decreased the serum concentrations of gonadotropin-releasing hormone (GnRH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone. It also decreased the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). Moreover, exposure to Cd resulted in decreased content of reduced glutathione (GSH) and total antioxidant capacity (T-AOC) concentrations, as well as increased malondialdehyde (MDA) and hydrogen peroxide (H₂O₂) contents. Cd also provoked testis autophagy by upregulating the expression of the autophagy-related proteins P62 and LC3 II. However, the combined administration of Nar and Cd significantly attenuated the Cd-induced negative effects by increasing the body weight, relative testis weights, and sperm quality and by decreasing testicular damage. Simultaneous supplementation of Nar and Cd markedly restored the decreased levels of GnRH, FSH, LH, testosterone, GSH, and T-AOC and the activities of SOD, CAT, and GPx caused by Cd treatment. Nar further suppressed MDA and H₂O₂ production and protected the testes from Cd-induced autophagy by downregulating P62 and LC3 II expression. Therefore, Nar protected the testes from Cd-induced toxicity.

本研究旨在研究柚皮素 (Nar) 对镉 (Cd) 诱导的睾丸毒性的影响。使用了 24 只 5 周龄的雄性 Sprague-Dawley (SD) 大鼠。给大鼠注射 0.9% NaCl（对照组）、CdCl ₂（腹膜内注射 2 毫克/千克体重）、Nar（50 毫克/千克体重，口服）和 CdCl ₂ + Nar（腹膜内注射 2 毫克/千克体重和口服 50 毫克/千克体重，分别为 4 周）。结果表明，镉处理组体重、睾丸相对重量和精子质量下降，镉在血清和睾丸中积累。病理检查表明Cd可引起睾丸损伤。Cd 降低促性腺激素释放激素 (GnRH)、促卵泡激素 (FSH)、促黄体激素 (LH) 和睾酮的血清浓度。它还降低了超氧化物歧化酶 (SOD)、过氧化氢酶 (CAT) 和谷胱甘肽过氧化物酶 (GPx) 的活性。此外，暴露于 Cd 导致还原型谷胱甘肽 (GSH) 含量和总抗氧化能力 (T-AOC) 浓度降低，以及丙二醛 (MDA) 和过氧化氢 (H ₂ O ₂） 内容。Cd 还通过上调自噬相关蛋白 P62 和 LC3 II 的表达来激发睾丸自噬。然而，通过增加体重、相对睾丸重量和精子质量以及减少睾丸损伤，Nar 和 Cd 的联合给药显着减弱了 Cd 引起的负面影响。同时补充Nar和Cd显着恢复了由Cd处理引起的GnRH、FSH、LH、睾酮、GSH和T-AOC水平的降低以及SOD、CAT和GPx的活性。Nar 进一步抑制 MDA 和 H ₂ O _{2 的}产生，并通过下调 P62 和 LC3 II 的表达来保护睾丸免受 Cd 诱导的自噬。因此，Nar 保护睾丸免受 Cd 诱导的毒性。