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Abstract This work showed for the first time the protective role of Naf, REBA, and Naf + REBA against MTX-induced testicular toxicity. The molecular protective mechanism includes: (1) Reducing oxidative stress caused by MTX by decreasing MDA level while increasing testicular SOD, CAT, and serum TAC; (2) Suppressing testicular inflammation by lowering inflammatory cytokines like IL-6 and TNF-α and suppressing NF-κB testicular immunostaining. (3) Inhibition of testicular apoptosis via downregulation of the apoptotic marker p53 and the apoptotic factor miR- 29a testicular expression (4) Upregulation of the cell proliferation marker Cdc42, which was implicated for the first time in MTX-induced gonadal toxicity protection. All of these actions resulted in marked testicular tissue injury alleviation and spermatogenesis improvement, which was evidenced by a significant increase in serum testosterone concentration and Johnsen’s score. For these reasons, pretreatment with Naf, REBA, and Naf + REBA could be utilized to reduce MTX gonadotoxicity. |