Prunin attenuates aflatoxin B1-induced testicular toxicity by alleviating oxidative stress and modulating TLR4/MyD88/NF-κB and Bax/Bcl-2/Caspase-3 signaling pathways.

Aflatoxin B1 (AFB1) is a mycotoxin that impairs the function of various vital organs of the body including testes. Prunin (PRU) is a plant derived flavonoid with potential pharmacological properties. The current research was performed to assess the potential role of PRU to counter AFB1-induced testicular toxicity in male albino rats. Forty-eight male rats (Weight: 230-250 g; Age: 8-10 week) were divided into four equal groups, including control, AFB1 (50 μg/kg) group, AFB1 + PRU (50 μg/kg + 20 mg/kg) co-treated group, and only PRU (20 mg/kg) group. The groups were treated with their respective doses for 56 days and then the rats were euthanized, samples were collected and biochemical as well as histopathological analyses were performed. The outcomes of our research showed that AFB1 upsurged the expressions of myeloid differentiation primary response 88 (MyD88), toll-like receptor 4 (TLR4), TNF receptor-associated factor 6 (TRAF6), and nuclear factor-kappa B (NF-κB). Moreover, AFB1 reduced the activities of antioxidant enzymes i.e., HO-1, GSR, GPx, CAT, SOD, while elevating ROS, MDA and inflammatory cytokines (TNF-α, IL-1β, COX-2 and IL-6) levels. AFB1 intoxicated group showed notable reduction in the HOS coiled tail sperms and spermatogenic indices i.e., sperm motility, count and viability. Furthermore, AFB1 increased the structural defects in mid-piece, head and tail of sperms and lowered the levels of testosterone. AFB1 also induced histological injuries in the testicles of rats. Additionally, AFB1 lowered the expressions of Bcl-2 and steroidogenic enzymes and increased the expressions of Caspase-3 and Bax. However, PRU supplementation markedly recovered the testicular tissues from AFB1-induced injuries. Our findings proposed that PRU exhibits the protective effects against AFB1-instigated testicular toxicity due to its oxidative stress mitigating and TLR4/NF-κB pathway modulating properties.