Nano-selenium Antagonizes Heat Stress-Induced Apoptosis of Rainbow Trout (Oncorhynchus mykiss) Hepatocytes by Activating the PI3K/AKT Pathway

被引:3
作者
Li, Lanlan [1 ]
Liu, Zhe [1 ]
Zhao, Guiyan [1 ]
Quan, Jinqiang [1 ]
Sun, Jun [1 ]
Lu, Junhao [1 ]
机构
[1] Gansu Agr Univ, Coll Anim Sci & Technol, 1 Yingmen Village, Lanzhou 730070, Gansu, Peoples R China
基金
中国国家自然科学基金;
关键词
Heat stress; Nano-selenium; Oxidative stress; Apoptosis; Primary hepatocytes; PI3K; AKT pathway; OXIDATIVE STRESS; MITOCHONDRIAL DYSFUNCTION; ANTIOXIDANT CAPACITY; TEMPERATURE; CELLS; EXPRESSION; TOXICITY; FISH;
D O I
10.1007/s12011-023-03637-9
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The cold-water fish rainbow trout (Oncorhynchus mykiss) shows poor resistance to heat, which is the main factor restricting their survival and yield. With the advancement of nanotechnology, nano-selenium (nano-Se) has emerged as a key nano-trace element, showing unique advantages, including high biological activity and low toxicity, for studying the response of animals to adverse environmental conditions. However, little is still known regarding the potential protective mechanisms of nano-Se against heat stress-induced cellular damage. Herein, we aimed to investigate the mechanism underlying the antagonistic effects of nano-Se on heat stress. Four groups were assessed: CG18 (0 mu g/mL nano-Se, 18 degrees C), Se18 (5.0 mu g/mL nano-Se, 18 degrees C), CG24 (0 mu g/mL nano-Se, incubated at 18 degrees C for 24 h and then transferred to 24 degrees C culture), and Se24 (5.0 mu g/mL nano-Se, incubated at 18 degrees C for 24 h and then transferred to 24 degrees C culture). We found that after heat treatment (CG24 group), T-AOC, GPx, and CAT activities in rainbow trout hepatocytes showed a decrease of 36%, 33%, and 19%, respectively, while ROS and MDA levels showed an increase of 67% and 93%, respectively (P < 0.05). Meanwhile, the mRNA levels of the apoptosis-related genes caspase3, caspase9, Cyt-c, Bax, and Bax/Bcl-2 in the CG24 group were 41%, 47%, 285%, 65%, and 151% higher than those in the CG18 group, respectively, while those of PI3K and AKT were 31% and 17% lower, respectively (P < 0.05). Besides, flow cytometry analysis showed an increase in the level of apoptotic cells after heat exposure. More importantly, we observed that nano-Se cotreatment (Se24 group) remarkably attenuated heat stress-induced effects (P < 0.05). We conclude that heat stress induces oxidative stress and apoptosis in rainbow trout hepatocytes. Nano-Se ameliorates heat stress-induced apoptosis by activating the PI3K/AKT pathway. Our results provide a new perspective to improve our understanding of the ability of nano-Se to confer heat stress resistance.
引用
收藏
页码:5805 / 5815
页数:11
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