食品与发酵工业 >

2024 , Vol. 50 >Issue 12: 53 - 62

DOI: https://doi.org/10.13995/j.cnki.11-1802/ts.036226

研究报告

扁舵鲣鱼低聚肽对HT-22细胞的神经保护和抗氧化作用

  • 赖育梅 ,
  • 吉宏武 ,
  • 陈铭 ,
  • 张迪 ,
  • 宋文奎 ,
  • 苏伟明
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  • 1(广东海洋大学 食品科技学院,广东省水产品加工与安全重点实验室,广东省海洋生物制品工程实验室,广东省海洋食品工程技术研究中心,水产品深加工广东普通高等学校重点实验室,广东 湛江,524088)
    2(海洋食品精深加工关键技术省部共建协同创新中心,大连工业大学,辽宁 大连,116034)
第一作者：硕士研究生(吉宏武教授为通信作者,E-mail:Jihw62318@163.com)

收稿日期: 2023-05-23

  修回日期: 2023-06-13

  网络出版日期: 2024-07-11

基金资助

国家重点研发计划课题(2019YFD0902000)

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Neuroprotective and antioxidant effects of Auxis thazard peptides on HT-22 cells

  • LAI Yumei ,
  • JI Hongwu ,
  • CHEN Ming ,
  • ZHANG Di ,
  • SONG Wenkui ,
  • SU Weiming
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  • 1(College of Food Science and Technology, Guangdong Ocean University, Guangdong Provincial Key Laboratory of Aquatic Products Processing and Safety, Guangdong Province Engineering Laboratory for Marine Biological Products, Guangdong Provincial Engineering Technology Research Center of Seafood, Key Laboratory of Advanced Processing of Aquatic Product of Guangdong Higher Education Institution, Zhanjiang 524088, China)
    2(Collaborative Innovation Center of Seafood Deep Processing, Dalian Polytechnic University, Dalian 116034, China)

Received date: 2023-05-23

  Revised date: 2023-06-13

  Online published: 2024-07-11

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摘要

为了评价扁舵鲣鱼低聚肽(Auxis thazard peptides,ATP)的神经保护作用和抗氧化作用,以皮质酮和谷氨酸为诱导剂构建HT-22细胞损伤模型,以细胞形态学、细胞活力、细胞功能和生化指标等指标探究扁舵鲣鱼低聚肽对HT-22损伤细胞的保护作用。结果表明,0.9 mmol/L的皮质酮和15.0 mmol/L的谷氨酸诱导HT-22细胞24 h,细胞存活率为50%左右。在该条件下,10、20、40 μg/mL的扁舵鲣鱼低聚肽均能显著抑制皮质酮和谷氨酸引起的HT-22细胞存活率下降,可提高血清素、乙酰胆碱酯酶和胆碱浓度,降低乙酰胆碱活性,抑制皮质酮诱导的细胞损伤,抑制谷氨酸诱导细胞产生的氧化应激,增加超氧化物歧化酶、谷胱甘肽酶与谷胱甘肽过氧化物酶的活性,减少氧化产物丙二醛和活性氧的产生。

关键词： 扁舵鲣鱼低聚肽; HT-22细胞; 乙酰胆碱; 神经保护; 抗氧化

本文引用格式

赖育梅 , 吉宏武 , 陈铭 , 张迪 , 宋文奎 , 苏伟明 . 扁舵鲣鱼低聚肽对HT-22细胞的神经保护和抗氧化作用[J]. 食品与发酵工业, 2024 , 50(12) : 53 -62 . DOI: 10.13995/j.cnki.11-1802/ts.036226

Abstract

This study aimed to evaluate the neuroprotective and antioxidant effects of Auxis thazard peptides (ATP) and to study the neuroprotective effect of ATP in the HT-22 cell injury model induced by corticosterone and glutamic acid.The protective effects of ATP on HT-22 injured cells were investigated based on cell morphology, cell viability, cell function, and biochemical indicators.Results showed that the cell viability of HT-22 cells induced by 0.9 mmol/L corticosterone and 15.0 mmol/L glutamic acid for 24 h was about 50%.Under these conditions, 10 μg/mL, 20 μg/mL, and 40 μg/mL ATP could significantly inhibit the decline in HT-22 cell viability induced by corticosterone and glutamic acid, increase the concentrations of serotonin, acetylcholinesterase and choline, reduce acetylcholine activity, inhibit cell damage induced by corticosterone, and inhibit oxidative stress induced by glutamic acid.The activities of superoxide dismutase, glutathione enzyme, and glutathione peroxidase were increased, and the production of oxidation products malondialdehyde and reactive oxygen species was decreased.

Key words： Auxis thazard peptides; HT-22 cell; acetylcholine; neuroprotection; antioxidation

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