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表没食子儿没食子酸酯对叔丁基过氧化氢诱导的黄羽肉鸡肝脏氧化应激的保护作用

Protective Effect of Epigallocatechin-3-gallate against Hepatic Oxidative Stress Induced by -Butyl Hhydroperoxide in Yellow-Feathered Broilers.

作者信息

Ma Xinyan, Ni Junli, Wang Wei, Zhu Yongwen, Zhang Yuqing, Sun Mingfei

机构信息

College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China.

Institute of Animal Science, Guangdong Academy of Agricultural Sciences, Guangzhou 510640, China.

出版信息

Antioxidants (Basel). 2024 Sep 24;13(10):1153. doi: 10.3390/antiox13101153.

Abstract

Recent studies have shown that epigallocatechin-3-gallate (EGCG), as an effective antioxidant, could attenuate the oxidative damage, inflammation and necrosis in the liver in response to oxidative stress. The present study investigated whether oral administration of EGCG could effectively alleviate the hepatic histopathological changes and oxidative damage in yellow-feathered broilers induced by -butyl hydroperoxide (-BHP). Broilers were exposed to 600 μmol -BHP/kg body weight (BW) to induce oxidative stress by intraperitoneal injection every five days, followed by oral administration of different doses of EGCG (0, 20, 40 and 60 mg/kg BW) and 20 mg vitamin E (VE)/kg BW every day during 5-21 days of age. The results showed that -BHP injection decreased ( < 0.05) body weight and the relative weight of the spleen; the enzyme activities of total antioxidant capacity (T-AOC), catalase (CAT) and total superoxide dismutase (SOD); and gene mRNA expressions of (), , , and ; as well as increased ( < 0.05) necrosis formation, malondialdehyde (MDA) content, reactive oxygen species (ROS)accumulation, and () mRNA expression in the liver of yellow-feathered female broilers at 21 days of age. Treatment with 60 mg EGCG/kg BW orally could enhance antioxidant enzyme activities and reverse the hepatic damage induced by -BHP injection by reducing the accumulation of ROS and MDA in the liver and activating the and pathways related to the induction of antioxidant gene expression ( < 0.05). In conclusion, intraperitoneal injection of -BHP impaired body growth and induced hepatic ROS accumulation, which destroyed the antioxidant system and led to oxidative damage in the liver of yellow-feathered broilers from 5 to 21 days of age. It is suggested that EGCG may play an antioxidant role through the and signaling pathways to effectively protect against -BHP-induced hepatic oxidative damage in broilers, and the appropriate dose was 60 mg EGCG/kg BW by oral administration.

摘要

近期研究表明,表没食子儿茶素没食子酸酯(EGCG)作为一种有效的抗氧化剂,可减轻肝脏因氧化应激而产生的氧化损伤、炎症和坏死。本研究调查了口服EGCG是否能有效缓解叔丁基过氧化氢(t-BHP)诱导的黄羽肉鸡肝脏组织病理学变化和氧化损伤。每隔五天给肉鸡腹腔注射600 μmol t-BHP/kg体重(BW)以诱导氧化应激,随后在5至21日龄期间每天口服不同剂量的EGCG(0、20、40和60 mg/kg BW)以及20 mg维生素E(VE)/kg BW。结果显示,注射t-BHP降低了(P<0.05)体重和脾脏相对重量;总抗氧化能力(T-AOC)、过氧化氢酶(CAT)和总超氧化物歧化酶(SOD)的酶活性;以及Nrf2、HO-1、CAT、SOD和GSH-Px的基因mRNA表达;同时增加了(P<0.05)21日龄黄羽肉种鸡肝脏中的坏死形成、丙二醛(MDA)含量、活性氧(ROS)积累以及Keap1 mRNA表达。口服60 mg EGCG/kg BW可增强抗氧化酶活性,并通过减少肝脏中ROS和MDA的积累以及激活与抗氧化基因表达诱导相关的Nrf2和HO-1途径,逆转t-BHP注射诱导的肝脏损伤(P<0.05)。总之,腹腔注射t-BHP损害了身体生长并诱导肝脏ROS积累,破坏了抗氧化系统,导致5至21日龄黄羽肉鸡肝脏发生氧化损伤。提示EGCG可能通过Nrf2和HO-1信号通路发挥抗氧化作用,有效保护肉鸡免受t-BHP诱导的肝脏氧化损伤,口服适宜剂量为60 mg EGCG/kg BW。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9952/11504997/1997cacbaf8a/antioxidants-13-01153-g001.jpg

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