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丙氨酸通过PI3K/AKT信号通路减轻脓毒症小鼠的肝损伤。

ALA Alleviates Liver Damage in Septic Mice Through PI3K/AKT Signaling Pathway.

作者信息

Song Yuqing, Mao Yuanrong, Sui Qingqing, Zhao Zichen, Dong Daosong

机构信息

Department of Pain The First Hospital of China Medical University Shenyang Liaoning People's Republic of China.

Department of Pain Qinghai Provincial People's Hospital Xining Qinghai People's Republic of China.

出版信息

Food Sci Nutr. 2025 Jul 10;13(7):e70599. doi: 10.1002/fsn3.70599. eCollection 2025 Jul.

Abstract

Sepsis is a life-threatening systemic inflammatory response syndrome that arises from infection and frequently progresses to multi-organ dysfunction, with liver injury being a particularly significant manifestation. Alpha-lipoic acid (ALA), renowned for its potent antioxidant and anti-inflammatory properties, has demonstrated promising protective effects in sepsis. The present study aims to investigate the protective effects of ALA on liver damage in septic mice by modulating the PI3K/AKT signaling pathway, thereby providing novel therapeutic strategies for the treatment of sepsis. The cecal ligation and puncture (CLP) model was employed to induce sepsis in mice, and both ALA-treated and control groups were established. The protective effects of ALA were evaluated through the detection of PI3K/AKT signaling pathway-related protein expression, apoptosis in liver cells, and liver function indicators. Additionally, Western blotting and immunohistochemistry were utilized to further validate ALA's regulatory impact on the PI3K/AKT signaling pathway. The study revealed that ALA significantly enhanced the activation of the PI3K/AKT signaling pathway, reduced apoptosis in liver cells of septic mice, and improved liver function indicators. Moreover, liver tissue pathology in the ALA-treated group was markedly less severe compared to that in the control group, indicating its effective hepatoprotective action. These findings demonstrate that ALA effectively alleviates liver damage in septic mice by promoting the PI3K/AKT signaling pathway, highlighting its potential clinical value. This research provides new targets and insights for the development of therapeutic strategies for sepsis.

摘要

脓毒症是一种由感染引起的危及生命的全身性炎症反应综合征,常进展为多器官功能障碍,肝损伤是其特别显著的表现。α-硫辛酸(ALA)以其强大的抗氧化和抗炎特性而闻名,已在脓毒症中显示出有前景的保护作用。本研究旨在通过调节PI3K/AKT信号通路来研究ALA对脓毒症小鼠肝损伤的保护作用,从而为脓毒症的治疗提供新的治疗策略。采用盲肠结扎和穿刺(CLP)模型诱导小鼠脓毒症,并设立ALA治疗组和对照组。通过检测PI3K/AKT信号通路相关蛋白表达、肝细胞凋亡和肝功能指标来评估ALA的保护作用。此外,利用蛋白质印迹法和免疫组织化学进一步验证ALA对PI3K/AKT信号通路的调节作用。研究发现,ALA显著增强了PI3K/AKT信号通路的激活,减少了脓毒症小鼠肝细胞的凋亡,并改善了肝功能指标。此外,与对照组相比,ALA治疗组的肝组织病理学明显较轻,表明其具有有效的肝保护作用。这些发现表明,ALA通过促进PI3K/AKT信号通路有效减轻脓毒症小鼠的肝损伤,突出了其潜在的临床价值。本研究为脓毒症治疗策略的开发提供了新的靶点和见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5c9/12245727/af919aa03ea2/FSN3-13-e70599-g001.jpg

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