Detection of Aflatoxin adducts as potential markers and the role of curcumin in alleviating AFB1-induced liver damage in chickens

Detection of Aflatoxin adducts as potential markers and the role of curcumin in alleviating AFB1-induced liver damage in chickens
复制标题

DOI:
10.1016/j.ecoenv.2019.03.089
复制
发表时间:
2019-07-30
影响因子:
6.8
通讯作者:
Zhang, Xiuying
Zhang, Xiuying
中科院分区:
环境科学与生态学2区
文献类型:
--
作者:
Li, Sihong;Muhammad, Ishfaq;Zhang, Xiuying

文献摘要

被引文献

相似文献

在本研究中,我们将黄曲霉毒素B_1加合物作为潜在的标志物,研究姜黄素通过抑制黄曲霉毒素B_1加合物的产生和AA肉鸡肝脏的氧化应激来减轻黄曲霉毒素B_1诱导的肝损伤。选用1日龄AA肉鸡,随机分为对照组、黄曲霉毒素B_1组(5 mg/kg黄曲霉毒素B_1)、黄曲霉毒素B_1+黄曲霉素组(300 mg/kg姜黄素+5 mg/kg黄曲霉素组)和姜黄素组(300 mg/kg)。对肉鸡血清生化指标、肝脏抗氧化能力、AFB1加合物及氧化应激机制进行了研究。黄曲霉毒素B_1治疗后出现肝损伤征象,表现为肝脏组织学损害,血清酶活性升高,肝脏抗氧化酶活性降低,ROS和8-OHdG活性降低。同时,AFB1抑制Nrf2/HO-1信号转导通路。免疫组织化学和酶联免疫吸附试验结果显示,黄曲霉毒素F1可显著增加小鼠肝脏AFB1-DNA加合物(p<0.05)和血清中AFB1-赖氨酸加合物(p<0.05)。重要的是,补充姜黄素可以改善这些变化。有趣的是,姜黄素通过抑制ROS、8-OHdG和AFB1加合物的产生,并激活Nrf2信号通路,减轻了AFB1诱导的毒性和氧化应激。总之,我们的实验表明,姜黄素可以被认为是一种潜在的预防黄曲霉毒素1诱导的毒性和氧化应激的药物,黄曲霉毒素1加合物可能是合适的治疗靶点。
In this study, we identified AFB1 adducts as potential markers and investigated the role of curcumin in alleviating AFB1-induced liver damage by suppressing the production of AFB1 adducts and oxidative stress in AA broilers liver. A total of 64 one-day-old Arbor Acres (AA) broilers were randomly divided into four groups, including control group, AFB1 group (5 mg/kg AFB1), cur + AFB1 group (300 mg/kg curcumin + 5 mg/kg AFB1) and curcumin group (300 mg/kg). Serum biochemical parameters, liver antioxidant abilities, AFB1 adducts and oxidative stress mechanism were studied in broilers. AFB1 administration accompany with signs of liver injury, including hepatic histological lesions, increased serum enzymes activities, decreased liver antioxidant enzymes activities and the suppression of ROS and 8-OHdG. Meanwhile, Nrf2/HO-1 pathway was depressed by AFB1 treatment. Immunohistochemistry and ELISA showed that AFB1 significantly increased AFB1-DNA adduct in liver (p < 0.05) and AFB1-lysine adduct in serum (p < 0.05). Importantly, supplementation of curcumin can ameliorate these alterations. Intriguingly, curcumin alleviated AFB1-induced toxicity and oxidative stress by inhibiting the generation of ROS, 8-OHdG and AFB1 adducts, and activated Nrf2 signaling pathway in broilers. Conclusively, our experiments suggest that curcumin could be considered as a potential agent for prevention of AFB1-induced toxicity and oxidative stress, and AFB1 adducts could be suitable therapeutic targets.