Here, we examined the protective effect of ferulic acid (FA) on cadmium chloride (CdCl₂)‐mediated reproductive toxicity in male rats. Animals were divided into four groups: control, FA (20 mg/kg), CdCl₂ (6.5 mg/kg), and FA + CdCl₂. CdCl₂ treatment evoked a significant increase in testis cadmium concentration in addition to obvious increase in testosterone, luteinizing hormone, and follicle‐stimulating hormone levels. Moreover, CdCl₂‐induced oxidative damage through exhausting the cellular defenses (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione) and downregulating the nuclear factor erythroid 2‐related factor 2 (Nrf2) expression accompanied by increases of malondialdehyde and nitric oxide contents. Testicular inflammation was evident indicated by increased levels of interleukin‐1β and tumor necrosis factor‐α in CdCl₂‐treated rats. CdCl₂ exposure also decreased the expression of the proliferating cell nuclear antigen and augmented apoptotic events associated with prominent histopathological alterations. However, FA coadministration mitigated the impaired hormonal level, apoptotic and inflammatory injuries elicited by CdCl_2, and maintained the oxidant/antioxidant balance in testicular tissue via Nrf2 activation.

中文翻译：

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阿魏酸影响Nrf2活化以恢复睾丸组织免受镉诱导的大鼠氧化反应，炎症和细胞凋亡

在这里，我们研究了阿魏酸（FA）对氯化镉（CdCl ₂）介导的雄性大鼠生殖毒性的保护作用。将动物分为四组：对照组，FA（20 mg / kg），CdCl ₂（6.5 mg / kg）和FA + CdCl ₂。CdCl ₂处理不仅显着增加睾丸激素，促黄体生成激素和刺激卵泡的激素水平，还引起睾丸镉浓度的显着增加。此外，CdCl ₂通过耗尽细胞防御能力（​​超氧化物歧化酶，过氧化氢酶，谷胱甘肽过氧化物酶，谷胱甘肽还原酶和谷胱甘肽）并下调核因子红系2相关因子2（Nrf2）的表达而引起氧化损伤，并伴有丙二醛和一氧化氮含量的增加。CdCl ₂处理的大鼠白细胞介素-1β和肿瘤坏死因子-α水平升高表明睾丸炎症明显。CdCl ₂暴露还降低了增殖细胞核抗原的表达，并增加了与明显的组织病理学改变相关的凋亡事件。但是，FA共同给药可减轻CdCl ₂引起的激素水平受损，凋亡和炎性损伤_。 并通过Nrf2激活维持睾丸组织中的氧化剂/抗氧化剂平衡。