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Protective Effect of Emodin against Hyperthermia‐induced Stress in Hepatic Cells of Grass Carp, Ctenopharyngodon idellus
- Liu, Bo, Cui, Yanting, Brown, Paul B., Xu, Pao, Wang, Aiming, Xie, Jun, Ge, Xianping
- Journal of the World Aquaculture Society 2016 v.47 no.3 pp. 424-434
- Ctenopharyngodon idella, cell viability, cultured cells, emodin, free radical scavengers, gene expression, heat shock proteins, heat stress, lactate dehydrogenase, membrane potential, messenger RNA, mitochondrial membrane, protective effect, reactive oxygen species, stress tolerance, temperature
- Emodin is an anthraquinone exhibiting several positive benefits of anti‐inflammatory, free radical scavenging, and resistance to stress. The goal of this study is to investigate the effects of emodin on the hepatic cell line of grass carp exposed to hyperthermic stress. Cultured cells were treated with various emodin concentrations (0, 0.04, 0.2, and 1.0 µg/mL) at 27 C for 24 h. Then all cultured cells were exposed to thermal stress by increasing the culture temperature (32 ± 0.5 C) for 0.5 h. Increased temperatures significantly reduced cell viability and increased lactate dehydrogenase (LDH) release in three of the four experimental groups (0, 0.2, and 1 µg/mL emodin) compared with the control. Additionally, reactive oxygen species (ROS) were significantly higher in cells exposed to elevated temperatures and treated with 0.2 or 1 µg/mL emodin and mitochondrial membrane potential was significantly lower in cells treated with 0, 0.2, or 1 µg/mL emodin. Expressions of heat shock proteins (HSP60, HSP70, and HSP90) were significantly higher in all but one of the experimental groups. Our results suggest that 0.04 µg/mL emodin can increase cell viability and HSP90 mRNA level, reduce LDH release and concentration of ROS, and contribute to enhance the resistance to high temperature stress in the hepatic cells of grass carp.