Here, we examined the protective effect of ferulic acid (FA) on cadmium chloride (CdCl 2)-mediated reproductive toxicity in male rats. Animals were divided into four groups: control, FA (20 mg/kg), CdCl 2 (6.5 mg/kg), and FA + CdCl 2. CdCl 2 treatment evoked a significant increase in testis cadmium concentration in addition to obvious increase in testosterone, luteinizing hormone, and follicle-stimulating hormone levels. Moreover, CdCl 2-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 CdCl 2-treated rats. CdCl 2 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. Practical applications Cadmium is an environmental toxicant and known to cause adverse effects including reproductive toxicity. However, antioxidant application has been found to protect against heavy metals-mediated toxic effects. Here, we examined the potential protective efficacy of ferulic acid against cadmium-mediated testicular impairments through estimating the amount of cadmium in the testis, hormonal profile, oxidative status, inflammatory response, apoptotic and proliferating markers in addition to the histopathological alterations. The obtained findings revealed that ferulic acid supplementation was able to abolish the testicular damages coupled with cadmium exposure. The protective efficiency of ferulic acid may correlated with its strong antioxidant, anti-inflammatory, and antiapoptotic activities; suggesting that ferulic acid may be used to ameliorate cadmium-induced testicular deficits. How to cite this article: Kassab RB, Lokman MS, Daabo HMA, et al. Ferulic acid influences Nrf2 activation to restore testicular tissue from cadmium-induced oxidative challenge, inflammation, and apoptosis in rats.

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Organophosphorus insecticide and growth regulator namely Ethephon (2-chloroethylphosphonic acid) are widely used as a ripening process accelerator and a cultivation duration inhibitor. Pomegranate extract (PPE) has recently been taken into consideration due to its pharmacological effects especially those associated with renal diseases. Thus, this study aims to investigate the possible protective effect of PPE against ethephon-induced nephrotoxicity in rats. In this study four groups of adult male rats were divided into control group, PPE 400 mg/kg group, Ethephon 250 mg/kg group, and finally, PPE + Ethephon group (treated with the same dose of PPE group and Ethephon group). In the current study, kidney function parameters (KIM-1, creatinine, and urea) along with oxidative stress markers, heme oxygenase-1 (HO-1) and nuclear factor erythroid 2–related factor 2 (Nrf2), glutathione (GSH) and its correlated enzymes, nitric oxide (NO), superoxide dismutase (SOD), malondialdehyde (MDA) and catalase (CAT) were estimated. Additionally, mediators of renal inflammation: interleukin 1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), nuclear factor kappa B (NF-κB) were measured. Apoptotic biomarkers (Bax, caspase 3, and Bcl2) in addition to renal histopathological data were also investigated. Results revealed that Ethephon elicited a significant increase in oxidation markers and reduced antioxidant levels, accompanied by oxidative renal tissue injury. Consequently, administration of Ethephon was reported to provoke secretion of the pro-inflammatory mediators. Moreover, histopathological results showed that deformities in the renal tissues were noticed which is attributed to Ethephon exposure. Interestingly, co-administration of PPE and Ethephon resulted in significantly ameliorated the biochemical and histopathological alterations produced by Ethephon. Current results propose the potential effect of PPE in the protection of renal tissue from Ethephon induced nephrotoxicity in rats.