文章摘要
热应激对大菱鲆心肌损伤及细胞凋亡的影响
Effect of thermal stress on turbot (Scophthalmus maximus) myocardial injury and apoptosis
投稿时间:2020-11-18  修订日期:2021-01-18
DOI:
中文关键词: 大菱鲆  热应激  心肌细胞  心脏  凋亡
英文关键词: turbot  thermal stress  Cardiomyocytes  heart  apoptosis
基金项目:现代农业产业技术体系专项, CARS-47-G01号;国家自然基金项目41706168;山东省良种工程, 2019LZGC013号;中国水产科学研究院基本科研业务费2020TD25; 烟台市科技计划项目2018ZDCX021.
作者单位邮编
郭晓丽 上海海洋大学水产与生命学院 上海
中国水产科学研究院黄海水产研究所 农业农村部海洋渔业可持续发展重点实验室 山东省海洋渔业生物技术与遗传育种重点实验室 青岛市海水鱼类种子工程与生物技术重点实验室 山东 青岛
青岛海洋科学与技术试点国家实验室海洋生物学与生物技术功能实验室 山东 青岛 
266071
黄智慧 中国水产科学研究院黄海水产研究所 农业农村部海洋渔业可持续发展重点实验室 山东省海洋渔业生物技术与遗传育种重点实验室 青岛市海水鱼类种子工程与生物技术重点实验室 山东 青岛 
马爱军 中国水产科学研究院黄海水产研究所 农业农村部海洋渔业可持续发展重点实验室 山东省海洋渔业生物技术与遗传育种重点实验室 青岛市海水鱼类种子工程与生物技术重点实验室 山东 青岛 266071
王庆敏 中国水产科学研究院黄海水产研究所 农业农村部海洋渔业可持续发展重点实验室 山东省海洋渔业生物技术与遗传育种重点实验室 青岛市海水鱼类种子工程与生物技术重点实验室 山东 青岛 
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中文摘要:
      大菱鲆作为一种低温适应冷水性经济鱼类,高温环境下严重影响其生长生存。该文为解析热应激对大菱鲆心脏损伤及其机制,从组织形态、生理生化反应及凋亡基因表达多个水平,开展相关研究。结果显示:随着温度升高,心肌纤维肿胀,断裂,间质宽度增加,炎细胞浸润,线粒体结构破坏等组织损伤现象加重,但在24℃-24h时组织损伤明显减轻;CK活性随着热应激加剧显著升高;LDH,SOD活性,MDA含量在24°C时达到峰值,表明大菱鲆遭受到热应激,心肌防御酶发挥抵抗作用,维持机体稳态。qPCR显示,大菱鲆心肌细胞 Bax 基因和Caspase-3基因变化趋势一致,随着热应激的加剧,表达量降低,而Bcl-2基因逐渐升高;表明在热应激程度较轻时,大菱鲆心肌通过降低Bax,Caspse-3基因表达,促进抗凋亡基因BCL-2的表达减少心肌细胞丢失来减少热应激损伤;当热应激加剧至28℃时,热应激超过自身生理调节阈值,损伤加重,机体防御系统自身也受损,造成大菱鲆心脏结构严重损伤甚至机体死亡。结果表明随着温度升高,大菱鲆心肌损伤加重,机体通过调节心肌防御酶活性以及细胞凋亡最大限度维持稳态减少组织损伤,超过24℃,则会造成机体损伤不可逆转地持续加重。本文为后续大菱鲆及其他鱼类心脏对热应激的生理适应性机制研究提供理论基础,同时为海洋鱼类耐高温性状选育提供更多的性状指标,提高选育精确性。
英文摘要:
      Turbot, as an economic fish adapted to cold water at low temperature, high temperature severely affects its growth and survival. The present study aimed to investigate in heart damage and mechanism the effects of thermal stress on physiologic, biochemical response and apoptosis gene expression multiple levels. The results showed that the aggravated degrees of swelling and breakage of myocardial fiber, dilatation of interstitial space, inflammatory cell infiltration, mitochondrial structure destruction and other tissue damage with the elevated temperature, but the tissue damage was significantly reduced at 24℃-24h. CK activity increased significantly with the escalation of heat stress; LDH, SOD activity and MDA content reach their peak at 24°C. Expression levels of Bax and Caspase-3 decreasing significantly after thermal tress, and the tendency were similar to them. However, the expression level of Bcl-2 gradually increased. These results indicated that the myocardium could reduce the expression of Bax and Caspse-3 genes and promote the expression of the anti-apoptotic gene Bcl-2 to reduce the loss of myocardial cells to reduce thermal stress damage when it suffered a lesser degree of heat stress. This suggested that turbot suffered thermal stress, which lead the heart defense enzymes to exert resistance to maintains body homeostasis. The organism defense system itself is damaged because the heat stress exceeds its own physiological regulation threshold when the heat stress intensifies to 28℃, which caused severely damages of heart structure and even lead to death in turbot. The results showed that thermal stress could cause myocardial damage of turbot, and the body maintains homeostasis via regulating the activity of defense enzymes and apoptosis pathway related genes. This study provides a theoretical basis for subsequent research of the physiological adaptation mechanism of turbot and other fishes heart to thermal stress. At the same time, it provides more trait indicators for the high temperature tolerance traits to improve the breeding accuracy of marine fish.
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