Wang Xujiao, Liu Xiao, Zhou Peng, Feng Jianguo, Jia Jing, Xie Bingqing, Chen Ye, Zhou Jun
Zigong Fourth People's Hospital, Zigong, 643000, Sichuan, China.
Anesthesiology and Critical Care Medicine Key Laboratory of Luzhou, Southwest Medical University, No. 25 Taiping Road, Jiangyang District, Luzhou, 646000, Sichuan, China.
Sci Rep. 2025 May 23;15(1):17901. doi: 10.1038/s41598-025-02891-2.
Hepatic encephalopathy (HE), a neuropsychiatric complication secondary to liver cirrhosis and hepatic failure, represents the leading cause of mortality in end-stage liver disease. While hyperammonemia remains the central pathogenic factor in HE progression, emerging evidence implicates oxidative stress, neuroinflammation, and neuronal apoptosis as critical synergistic contributors to HE pathogenesis. Hydrogen-rich water, known for its antioxidant, anti-inflammatory, and anti-apoptotic properties, has not been systematically investigated for therapeutic efficacy in HE management. In the current investigation, we successfully established a HE rat model by administering thioacetamide via intraperitoneal injection. By observing the general state and behavioral changes of the rats, detecting liver function and blood ammonia, and observing the pathological changes of liver and brain tissue, it was discussed whether hydrogen-rich water had a preventive and therapeutic effect on hepatic encephalopathy. Oxidative stress, inflammation and neuronal apoptosis were detected in plasma, prefrontal cortex and hippocampus to explore the possible mechanism of its protective effect. The results showed that hydrogen-rich water can improve the behavioral changes of the HE rats, reduce blood ammonia, reduce liver function damage, alleviate the pathological changes of liver and brain tissue, significantly inhibit the systemic and local oxidative stress and inflammation of the brain tissue of the HE rats, and reduce neuronal apoptosis. In summary, hydrogen-rich water might stabilize liver-brain disturbance in thioacetamide-induced HE rats by anti-inflammation, anti-oxidative stress and reducing neuronal apoptosis.
肝性脑病（HE）是肝硬化和肝衰竭继发的神经精神并发症，是终末期肝病死亡的主要原因。虽然高氨血症仍然是HE进展的核心致病因素，但新出现的证据表明氧化应激、神经炎症和神经元凋亡是HE发病机制的关键协同因素。富氢水以其抗氧化、抗炎和抗凋亡特性而闻名，但尚未对其在HE治疗中的疗效进行系统研究。在本研究中，我们通过腹腔注射硫代乙酰胺成功建立了HE大鼠模型。通过观察大鼠的一般状态和行为变化、检测肝功能和血氨，并观察肝脏和脑组织的病理变化，探讨富氢水对肝性脑病是否具有防治作用。检测血浆、前额叶皮质和海马中的氧化应激、炎症和神经元凋亡，以探讨其保护作用的可能机制。结果表明，富氢水可改善HE大鼠的行为变化，降低血氨，减轻肝功能损害，缓解肝脏和脑组织的病理变化，显著抑制HE大鼠脑组织的全身和局部氧化应激及炎症反应，减少神经元凋亡。综上所述，富氢水可能通过抗炎、抗氧化应激和减少神经元凋亡来稳定硫代乙酰胺诱导的HE大鼠的肝脑紊乱。
