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陈付菊, 付生云, 马敏, 常兰, 李雪源. 低氧胁迫对青海湖裸鲤端脑抗氧化酶活性、细胞凋亡及相关基因表达的影响[J]. 水生生物学报, 2023, 47(4): 572-580. DOI: 10.7541/2023.2021.085
引用本文: 陈付菊, 付生云, 马敏, 常兰, 李雪源. 低氧胁迫对青海湖裸鲤端脑抗氧化酶活性、细胞凋亡及相关基因表达的影响[J]. 水生生物学报, 2023, 47(4): 572-580. DOI: 10.7541/2023.2021.085
CHEN Fu-Ju, FU Sheng-Yun, MA Min, CHANG Lan, LI Xue-Yuan. HYPOXIA STRESS ON THE ACTIVITY OF ANTIOXIDANT ENZYMES, NEURONAL APOPTOSIS AND EXPRESSION OF RELATED GENES OF TELENCEPHALON IN GYMNOCYPRIS PRZEWALSKII[J]. ACTA HYDROBIOLOGICA SINICA, 2023, 47(4): 572-580. DOI: 10.7541/2023.2021.085
Citation: CHEN Fu-Ju, FU Sheng-Yun, MA Min, CHANG Lan, LI Xue-Yuan. HYPOXIA STRESS ON THE ACTIVITY OF ANTIOXIDANT ENZYMES, NEURONAL APOPTOSIS AND EXPRESSION OF RELATED GENES OF TELENCEPHALON IN GYMNOCYPRIS PRZEWALSKII[J]. ACTA HYDROBIOLOGICA SINICA, 2023, 47(4): 572-580. DOI: 10.7541/2023.2021.085

低氧胁迫对青海湖裸鲤端脑抗氧化酶活性、细胞凋亡及相关基因表达的影响

HYPOXIA STRESS ON THE ACTIVITY OF ANTIOXIDANT ENZYMES, NEURONAL APOPTOSIS AND EXPRESSION OF RELATED GENES OF TELENCEPHALON IN GYMNOCYPRIS PRZEWALSKII

  • 摘要: 为研究青海湖裸鲤(Gymnocypris przewalskii)端脑在低氧胁迫下的生理响应机制, 选取体重(97.68±0.12) g、体长(24.11±0.12) cm的健康青海湖裸鲤进行低氧溶解氧含量(0.7±0.1) mg/L胁迫, 设常氧溶解氧含量(8.4±0.1) mg/L为对照组, 分别在低氧胁迫8h和24h时采集青海湖裸鲤的端脑组织, 进行脑细胞线粒体超微结构和膜电位、抗氧化酶活性、脑细胞凋亡和凋亡相关基因(Caspase 3BaxBcl-2)及低氧诱导反应相关基因(Hif-2αEGLN1)表达测定。结果显示, 在低氧胁迫过程中: (1)端脑神经细胞线粒体出现肿胀、嵴溶解; 线粒体膜电位在8h时显著升高, 24h时显著降低, 表明随着低氧胁迫时间的延长端脑神经细胞线粒体可能受到了损伤。(2)TUNEL检测显示端脑细胞发生了凋亡, 但随着低氧胁迫时间延长端脑细胞凋亡率无显著差异; qPCR显示, 随着低氧胁迫时间的延长端脑细胞Caspase 3BaxBcl-2基因表达水平升高; Bcl-2/Bax比值随低氧胁迫时间的延长显著降低; Hif-2α基因表达水平显著升高; EGLN1基因表达水平显著降低。(3)分光光度法结果显示, 端脑细胞过氧化氢(H2O2)含量在8h时显著增加, 但随着低氧胁迫时间延长H2O2含量无显著差异; 超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量和总抗氧化能力(T-AOC)在8h时与常氧组无显著差异, 24h时显著高于常氧组; 谷胱甘肽过氧化物酶(GPX)组间无显著差异。以上结果提示, 低氧胁迫通过促进端脑细胞ROS产生, 改变线粒体膜的通透性, 上调Caspase 3BaxBcl-2基因表达, 导致端脑细胞凋亡。同时, 在低氧胁迫下端脑细胞可能通过提高T-AOC和SOD活性及上调Hif-2α基因和下调EGLN1基因表达来减少低氧应激对端脑细胞的损伤。

     

    Abstract: To explore the physiological response of Qinghai Lake naked carp (Gymnocypris przewalskii) telencephalon cells to hypoxia, the carp with body weight (97.68±0.12) g and body length (24.11±0.12) cm were challenged with hypoxia stress dissolved oxygen content of (0.7±0.1) mg/L and normoxia dissolved oxygen content of (8.4±0.1) mg/L for 24h to measure mitochondrial ultrastructure, membrane potential, antioxidant enzyme activities, telencephalon cells apoptosis, apoptotic-related genes (Caspase 3, Bax and Bcl-2) and hypoxia-induced response-related gene (Hif-2α and EGLN1). The results showed that: (1) nerve cells mitochondria swelled and their cristae dissolved during hypoxia stress, the mitochondrial membrane potential increased significantly at 8h and then significantly decreased at 24h, indicating the destroyed mitochondria of telencephalon cells with the increased hypoxia time. (2) hypoxia enhanced cell apoptosis and the expression levels of Caspase 3, Hif-2α, Bax and Bcl-2 genes in telencephalon cells, and significantly decreased the ratio of Bcl-2/Bax and the expression of EGLN1. (3) the increased content of hydrogen peroxide (H2O2) in telencephalon cells only happened at 8h. Hypoxia significantly induced the activity of superoxide dismutase (SOD), the content of malondialdehyde (MDA) and the total antioxidant capacity (T-AOC) only at 24h. Furthermore, there was no significant difference in glutathione peroxidase (GPX) between the groups. These results suggest that hypoxia stress mediates the permeability of mitochondrial membrane and the expression of Caspase 3, Bax and Bcl-2 genes via ROS production in telencephalon cells to induce telencephalon cells apoptosis, which might be balanced by increasing the activities of T-AOC and SOD and the expression levels of Hif-2α and decreasing the expression levels of EGLN1.

     

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