详细信息
文献类型:期刊文献
英文题名:Alleviative Effect of Threonine on Cadmium-Induced Liver Injury in Mice
作者:Fang, Zhijia[1,2,3,4,5];Li, Yongbin[1,2,3,4,5];Wang, Jingwen[1,2,3,4,5];Wang, Xinran[1,2,3,4,5];Huang, Linru[1,2,3,4,5];Sun, Lijun[1,2,3,4,5];Deng, Qi[1,2,3,4,5]
机构:[1]Guangdong Ocean Univ, Coll Food Sci & Technol, 1 Haida Rd, Zhanjiang 524088, Guangdong, Peoples R China;[2]Guangdong Prov Key Lab Aquat Prod Proc & Safety, Zhanjiang, Peoples R China;[3]Guangdong Prov Engn Lab Marine Biol Prod, Zhanjiang, Peoples R China;[4]Guangdong Prov Engn Technol Res Ctr Seafood, Zhanjiang, Peoples R China;[5]Guangdong Higher Educ Inst, Key Lab Adv Proc Aquat Prod, Zhanjiang 524088, Peoples R China
年份:2023
卷号:201
期号:9
起止页码:4437
外文期刊名:BIOLOGICAL TRACE ELEMENT RESEARCH
收录:SCI-EXPANDED(收录号:WOS:000914668700001)、、Scopus(收录号:2-s2.0-85143239344)、WOS
基金:This work was supported by the National Natural Science Foundation of China (No. 32172215 and 31701706), Guangdong Basic and Applied Basic Research Foundation (No. 2019A1515010809 and 2021A1515012443).
语种:英文
外文关键词:Cadmium; Threonine; Liver injury; Oxidative damage; Inflammatory factor; Apoptosis
外文摘要:As a toxic trace element commonly found in food, cadmium (Cd) can cause severe liver injury. Our previous study showed that threonine (Thr) could significantly alleviate Cd toxicity in yeast. To investigate the effect of Thr on Cd-induced liver injury in mice, twenty-four mice were randomly divided into four groups: control, Cd, and low/high dose of Thr-treatment groups (0.04 and 0.08 mmol/kg/day, respectively). After 7 days of continuous treatment, the alleviative effect of Thr on liver injury in Cd-exposed mice was assessed. The results showed that Thr significantly reduced the elevation of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in Cd-exposed mice. Histological analysis showed that Thr decreased Cd-induced hepatic steatosis, zonal necrosis, and inflammatory cell infiltration. Thr also reduced the Cd-induced malondialdehyde (MDA) and O2- levels and restored superoxide dismutase (SOD) and catalase (CAT) activities in the liver. Further investigation showed that Thr significantly suppressed Cd-induced inflammatory response (tumor necrosis factor-alpha and interleukin-6) and restored the level of anti-apoptotic protein (Blc-2) but inhibited the elevation of pro-apoptotic proteins (Bax and caspase-3), as well as the activation of the PI3K/AKT signaling pathway in Cd-exposed mice. In conclusion, Thr alleviated Cd-induced liver injury through reducing Cd-induced oxidative stress, inflammation, and attenuating hepatocyte apoptosis via PI3K/AKT-related signaling pathway.
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