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<p>Long-term psychological stress is associated with increased intestinal epithelial permeability. In the human central nervous system, gamma-aminobutyric acid (GABA), a non-protein amino acid found in bacteria, plants, and animals, acts as an inhibitory neurotransmitter that controls the cardiovascular system, reduces blood pressure, enhances mood, and encourages sleep. It is still unclear how GABA controls the function of the colon epithelial barrier under long-term stress. This study explored the potential of GABA to ameliorate cortisol-induced damage in human colorectal adenocarcinoma cells (HT29) and the mechanisms at play. Our results indicate that GABA mitigated cellular damage by neutralizing the negative impacts of Cortisol on HT29 cell viability, permeability, and the expression of barrier-associated proteins. Additionally, GABA maintained the cellular barrier function and antioxidant defense. Overall, our results point to the possibility that GABA may shield HT29 cells from harm caused by cortisol by activating the Nrf2 signaling pathway.</p>

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Gamma-aminobutyric acid attenuates cortisol-induced damage in human colorectal adenocarcinoma cells via Nrf2 signaling

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年10月20日

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  • Yijie Liu ,
  • Yue Wu

摘要

Long-term psychological stress is associated with increased intestinal epithelial permeability. In the human central nervous system, gamma-aminobutyric acid (GABA), a non-protein amino acid found in bacteria, plants, and animals, acts as an inhibitory neurotransmitter that controls the cardiovascular system, reduces blood pressure, enhances mood, and encourages sleep. It is still unclear how GABA controls the function of the colon epithelial barrier under long-term stress. This study explored the potential of GABA to ameliorate cortisol-induced damage in human colorectal adenocarcinoma cells (HT29) and the mechanisms at play. Our results indicate that GABA mitigated cellular damage by neutralizing the negative impacts of Cortisol on HT29 cell viability, permeability, and the expression of barrier-associated proteins. Additionally, GABA maintained the cellular barrier function and antioxidant defense. Overall, our results point to the possibility that GABA may shield HT29 cells from harm caused by cortisol by activating the Nrf2 signaling pathway.