叔丁基氢醌(tBHQ)已成为减轻T-2引起的生殖毒性的不利影响的有希望的候选者。tBHQ对大鼠精子质量的保护作用,睾丸损伤,凋亡,并对T-2毒素暴露诱导的炎症进行了研究。睾丸组织的组织病理学检查显示T-2治疗组严重损伤,以生殖细胞排列混乱为特征,扭曲的生灵小管壁变薄,和显著的细胞坏死。然而,tBHQ管理,作为预防或治疗措施,减轻了这种结构损伤。图像分析证实,与T-2治疗组相比,tBHQ治疗组的曲细小管的横截面积和高度增加(p<0.05),表明tBHQ在减轻睾丸损伤方面的功效。此外,tBHQ处理显著抑制T-2诱导的睾丸组织细胞凋亡,如显示凋亡细胞计数减少和BAX/BCL2比率和caspase-3表达下调的结果所证明的(p<0.05)。tBHQ显著增加了抗氧化因子SOD的浓度,CAT,TAC,和GSH-PX。此外,tBHQ减弱了T-2暴露诱导的炎症反应,正如促炎细胞因子Tnf的mRNA表达降低所表明的那样,睾丸组织中的Il1和Il10(p<0.05)。此外,tBHQ治疗减轻T-2诱导的血清睾酮下降,促进睾酮合成基因表达,包括17β-HSD和Cyp11a1基因,在大鼠睾丸中(p<0.05)。这些发现强调了tBHQ作为对抗T-2诱导的生殖毒性的治疗剂的作用,强调它的抗氧化作用,抗凋亡,和抗炎特性。进一步阐明tBHQ的作用机制可能为预防和治疗环境毒素引起的生殖障碍提供新的策略。
Tert-butylhydroquinone (tBHQ) has emerged as a promising candidate for mitigating the adverse effects of T-2-induced reproductive toxicity. The protective effects of tBHQ on rat sperm quality, testicular injury, apoptosis, and inflammation induced by T-2 toxin exposure were investigated. Histopathological examination of testicular tissues revealed severe damage in the T-2-treated group, characterized by disorganized germ cell arrangement, thinning of the convoluted seminiferous tubule walls, and significant cellular necrosis. However, tBHQ administration, either as a preventive or therapeutic measure, mitigated this structural damage. Image analysis confirmed an increase in the cross-sectional area and height of the convoluted seminiferous tubules in the tBHQ-treated groups compared to the T-2-treated group (p < 0.05), indicating tBHQ\'s efficacy in alleviating testicular damage. Additionally, tBHQ treatment significantly inhibited T-2-induced apoptosis of testicular tissue cells, as evidenced by the results showing reduced apoptotic cell counts and downregulation of the BAX/BCL2 ratio and caspase-3 expression (p < 0.05). tBHQ significantly increased the concentrations of the antioxidant factors SOD, CAT, TAC, and GSH-PX. Furthermore, tBHQ attenuated the inflammatory response induced by T-2 exposure, as indicated by the decreased mRNA expression of the proinflammatory cytokines Tnf, Il1, and Il10 in testicular tissue (p < 0.05). Additionally, tBHQ treatment alleviated the decline in serum testosterone induced by the T-2 and promoted testosterone synthesis gene expression, including for the genes 17β-HSD and Cyp11a1, in rat testes (p < 0.05). These findings underscore tBHQ\'s role as a therapeutic agent combatting T-2-induced reproductive toxicity, highlighting its antioxidative, anti-apoptotic, and anti-inflammatory properties. Further elucidation of tBHQ\'s mechanisms of action may offer novel strategies for preventing and treating reproductive disorders induced by environmental toxins.