叔丁基对苯二酚通过抗氧化应激和抗凋亡作用减轻T-2毒素诱导的雄性大鼠肾毒性OA
Tertiary Butylhydroquinone(TBHQ)Mitigates T-2 Toxin-induced Nephrotoxicity in Male Rats(Rattus norvegicus)via Anti-oxidative Stress and Anti-apoptotic Effects
T-2毒素为谷物及饲料中常见的高毒性镰刀菌(Fusarium)毒素,可通过诱导氧化应激和线粒体功能障碍激活细胞凋亡通路并造成重要脏器损伤,其中肾脏作为毒物代谢与排泄的关键器官更易受到攻击,然而针对其肾毒性的有效防护策略仍有限.叔丁基对苯二酚(tertiary butylhydroquinone,TBHQ)作为酚类抗氧化剂,可激活Nrf2/HO-1通路并拮抗氧化应激和凋亡,本研究拟通过评估TBHQ对T-2毒素诱导的雄性大鼠肾毒性的保护作用,探讨其分子机制.将40只SD雄性大鼠(Rattus norvegicus)随机分为空白组、T-2组(仅给予T-2毒素)、TBHQ预处理组(TBHQ+T-2组:先腹腔注射TBHQ 14 d,后灌胃T-2毒素7 d)和M组(同时给予TBHQ和T-2毒素 7 d).实验末期,测定大鼠血清生化指标(SCR,Cys-C,β2-MG)、肾组织氧化应激指标(SOD,CAT,GSH-PX,TAC,MDA)、抗氧化基因(Sod,Cat,Gpx)表达、组织病理学损伤(HE,Masson,PAS染色)及细胞凋亡率(TUNEL).结果显示,与空白组相比,T-2组大鼠血清SCR和Cys-C显著升高(P＜0.05),肾脏SOD、MDA含量和细胞凋亡率显著增加(P＜0.05),肾组织结构严重受损.与T-2组相 比,TBHQ预处理可显著降低血清肾功能指标(P＜0.05),降低MDA含量(P＜0.05),显著上调Gpx mRNA表达(P＜0.05),极显著降低细胞凋亡率(P＜0.01),并明显改善肾脏组织结构损伤.TBHQ预处理组的保护效果优于M组.TBHQ通过增强抗氧化应激和抗凋亡作用,减轻T-2毒素对雄性大鼠的肾脏损伤,且预处理的保护效果更佳.本研究为阐明T-2毒素肾毒性的氧化应激-凋亡机制提供了实验依据,并为饲料霉菌毒素相关肾损伤的预防性保护措施提供理论参考.
T-2 toxin is a highly toxic Fusarium toxin commonly found in grains and feed.It can activate apoptosis pathways by inducing oxidative stress and mitochondrial dysfunction,and damage important organs.The kidney,as a key organ for toxin metabolism and excretion,is more vulnerable to attack.However,effective protective strategies against its nephrotoxicity are still limited.As a phenolic antioxidant,tertiary butylhydroquinone(TBHQ)can activate the Nrf2/HO-1 pathway and counteract oxidative stress and apoptosis.Therefore,this study aims to investigate the protective effect of TBHQ against T-2 toxin-induced nephrotoxicity in male rats and to explore its molecular mechanisms.40 male SD rats(Rattus norvegicus)were divided into Control group,T-2 group(T-2 toxin only),TBHQ+T-2 group(TBHQ i.p.for 14 d,followed by T-2 gavage for 7 d),and M group(simultaneous TBHQ and T-2 for 7 d).End-point analysis included serum markers(SCR,Cys-C,β2-MG),renal oxidative stress(SOD,CAT,GSH-PX,TAC,MDA),antioxidant gene expression(Sod,Cat,Gpx),histopathology(HE,Masson,PAS staining),and the cell apoptosis rate(TUNEL).The results showed that compared with Control group,serum levels of SCR and Cys-C were significantly elevated in rats of the T-2 group(P＜0.05);renal SOD and MDA contents as well as the renal cell apoptosis rate were significantly increased(P＜0.05),accompanied by damage to renal structure.However,TBHQ pretreatment significantly reversed these pathological changes:It reduced serum renal markers and MDA content(P＜0.05),markedly reduced cell apoptosis(P＜0.01),significantly improved histopathological lesions,and upregulated the mRNA expression of antioxidant genes Gpx(P＜0.05)compared with the T-2 group.Furthermore,the protective effect of the TBHQ pretreatment regimen was superior to the M group.In conclusion,TBHQ mitigated T-2 toxin-induced renal injury in male rats by enhancing its anti-oxidative stress and anti-apoptotic effects,with pretreatment offering a more effective strategy.This study provides experimental evidence for elucidating the oxidative stress apoptosis mechanism of T-2 toxin nephrotoxicity as well as theoretical references for preventive protective measures against feed mycotoxin related kidney injury.
陈淑妍;黎源;刘雨晴;陈丽圆;陈清桦;唐胜球;陈云
韶关学院 生物与农业学院,韶关 512005韶关学院 生物与农业学院,韶关 512005韶关学院 生物与农业学院,韶关 512005韶关学院 生物与农业学院,韶关 512005韶关学院 生物与农业学院,韶关 512005韶关学院 生物与农业学院,韶关 512005||韶关学院 广东省粤北食药资源利用与保护重点实验室,韶关 512005韶关学院 生物与农业学院,韶关 512005||韶关学院 广东省粤北食药资源利用与保护重点实验室,韶关 512005
农业科技
叔丁基对苯二酚(TBHQ)T-2毒素肾脏损伤雄性大鼠凋亡
Tertiary butylhydroquinone(TBHQ)T-2 toxinKidney injuryMale ratApoptosis
《农业生物技术学报》 2026 (7)
1495-1505,11
省级大学生创新创业训练计划(S202410576034)广东省基础与应用基础研究基金(2024A1515013150)广东省普通高校特色创新项目(2024KTSCX068)2023年度韶关市支持科研工作者项目(230324108035353)2024年度韶关市支持科研工作者项目(P0000876050)
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