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生化、组织学和多组学分析揭示中华鳖冷应激反应的分子和代谢机制。

Biochemical, Histological, and Multi-Omics Analyses Reveal the Molecular and Metabolic Mechanisms of Cold Stress Response in the Chinese Soft-Shelled Turtle ().

作者信息

Ji Liqin, Shi Qing, Chen Chen, Liu Xiaoli, Zhu Junxian, Hong Xiaoyou, Wei Chengqing, Zhu Xinping, Li Wei

机构信息

Key Laboratory of Tropical and Subtropical Fishery Resources Application and Cultivation, Ministry of Agriculture and Rural Affairs, Pearl River Fisheries Research Institute, Chinese Academy of Fishery Sciences, Guangzhou 510380, China.

出版信息

Biology (Basel). 2025 Jan 11;14(1):55. doi: 10.3390/biology14010055.

DOI:10.3390/biology14010055
PMID:39857286
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11760877/
Abstract

The Chinese soft-shelled turtle (), a type of warm-water reptile, is frequently chosen as the model animal to understand how organisms respond to environmental stressors. However, the responsive mechanism of to natural cold stress is unclear, especially in terms of metabolic pattern and molecular pathways. Herein, plasma biochemical, hepatic morphological, apoptotic, transcriptomic, and metabolomic detection methods were performed to investigate the response of to acute cold stress. A consistent increase in plasma AST and ALT activities with a decline in ALP activity was found following 14 °C and 7 °C cold stress compared with the control group. Plasma GLU, TG, CHO, and HDL contents, reflecting energy metabolism, were decreased to lower levels from 2 to 16 days post cold stress (dps). Histological and TUNEL detection in the liver demonstrated that the 14 °C and 7 °C cold stress caused severe morphological damage and cell apoptosis in a time-dependent manner. DEGs in the biosynthesis of fatty acids ( and ), as well as unsaturated fatty acids (, , , and ), starch and sucrose metabolism (, , and ), and apoptosis (, , , , , , , , and ) were discovered in the transcriptome under cold stress. The metabolomic data showed that metabolites, including chenodeoxycholic acid, oleoylethanolamide, uric acid, fructose 1,6-bisphosphate, CMP, and S-(Hydroxymethyl)-glutathione, were remarkably altered in the cold stress groups. Combined transcriptomic and metabolomic data revealed that pyrimidine metabolism, amino acid metabolism, and pyruvate metabolism were the most significant pathways regulated by the low-temperature exposure. Overall, this work suggests that 14 °C and 7 °C cold stress could induce obvious morphological damage and apoptosis in the liver at 4 dps. Moreover, energy metabolism and amino acid metabolism were the main signaling pathways in response to cold stress for .

摘要

中华鳖是一种温水性爬行动物,常被选作模式动物来研究生物体如何应对环境应激源。然而,中华鳖对自然低温应激的响应机制尚不清楚,尤其是在代谢模式和分子途径方面。在此,采用血浆生化、肝脏形态学、凋亡、转录组学和代谢组学检测方法,研究中华鳖对急性低温应激的反应。与对照组相比,在14℃和7℃低温应激后,血浆AST和ALT活性持续升高,而ALP活性下降。反映能量代谢的血浆GLU、TG、CHO和HDL含量在低温应激后2至16天降至较低水平。肝脏的组织学和TUNEL检测表明,14℃和7℃低温应激以时间依赖的方式导致严重的形态损伤和细胞凋亡。在低温应激下的转录组中发现了脂肪酸(和)、不饱和脂肪酸(、、、和)生物合成、淀粉和蔗糖代谢(、、和)以及凋亡(、、、、、、、、和)中的差异表达基因(DEGs)。代谢组学数据显示,包括鹅去氧胆酸、油酰乙醇胺、尿酸、1,6-二磷酸果糖、CMP和S-(羟甲基)-谷胱甘肽在内的代谢物在低温应激组中发生了显著变化。转录组学和代谢组学数据相结合表明,嘧啶代谢、氨基酸代谢和丙酮酸代谢是低温暴露调节的最显著途径。总体而言,这项研究表明,14℃和7℃低温应激在4天时可诱导肝脏明显的形态损伤和凋亡。此外,能量代谢和氨基酸代谢是中华鳖应对低温应激的主要信号通路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd0/11760877/14ca559b84f2/biology-14-00055-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd0/11760877/778865bf93d0/biology-14-00055-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd0/11760877/6d4dd5a2e38b/biology-14-00055-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd0/11760877/14ca559b84f2/biology-14-00055-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd0/11760877/778865bf93d0/biology-14-00055-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd0/11760877/044ed167cfbf/biology-14-00055-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd0/11760877/07d686e919b9/biology-14-00055-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd0/11760877/c2a7642abefa/biology-14-00055-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd0/11760877/4418c7520d5d/biology-14-00055-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd0/11760877/0f6d71cbe3b3/biology-14-00055-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd0/11760877/3075adefd384/biology-14-00055-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd0/11760877/14ca559b84f2/biology-14-00055-g009.jpg

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