Effects of zingerone on rat induced testicular toxicity by sodium arsenite via oxidative stress, endoplasmic reticulum stress, inflammation, apoptosis, and autophagy pathways

Objective(s): This study aimed to investigate the effects of zingerone (ZNG) treatment on testicular toxicity in rats induced by sodium arsenite (SA).Materials and Methods: In the study, five groups were formed (n=۷) and the experimental groups were designated as follows; Vehicle group, ZNG group, SA group, SA+ZNG ۲۵ group, and SA+ZNG ۵۰ group. While SA was administered orally to rats at ۱۰ mg/kg/bw, ZNG was given to rats orally at ۲۵ and ۵۰ mg/kg/bw doses for ۱۴ days.Results: As a result of the presented study, an increase was observed in the MDA contents of the testicular tissue of the rats administered SA, while significant decreases were observed in GSH levels, SOD, CAT, and GPx activities. The mRNA transcript levels of the pro-inflammatory genes NF-κB, TNF-α, IL-۱β, and IL-۶ were triggered after SA administration. Additionally, SA administration caused inflammation by increasing RAGE, NLRP۳, and JAK-۲/STAT۳ gene expression. Moreover, endoplasmic reticulum (ER) stress occurred in the testicular tissues of SA-treated rats and thus ATF-۶, PERK, IRE۱, and GRP۷۸ genes were up-regulated. SA caused apoptosis by up-regulating Bax and Caspase-۳ expressions and inhibiting Bcl-۲ expression in testicles. SA caused histological irregularities in the testicles, resulting in decreased sperm quality.Conclusion: ZNG treatment reduced SA-induced oxidative stress, ER stress, inflammation, apoptosis, and histological irregularities in the testicles while increasing sperm quality. As a result, it was observed that ZNG could alleviate the toxicity caused by SA in the testicles.

کلیدواژه ها:

Apoptosis ، Inflammation ، Oxidative stress ، Sodium arsenite ، Testicular toxicity