氢气对脂肪肝、肝脏缺血再灌注损伤、胆管结扎引起的肝脏损伤、肝脏器官移植损伤等都发现具有理想的治疗效果，但对慢性肝脏疾病的纤维化并没有开展系统研究，本研究采用多种肝脏损伤模型，结合部分细胞血研究，证明氢气对四氯化碳、硫代乙酰胺诱导的肝纤维化有明显抑制作用，细胞血证据表明这种作用和氢气对肝细胞内羟自由基的清除有关。这一研究来自日本京都大学,医学院外科学系，文章发表在HepatologyResearch上。

肝脏纤维化是慢性肝脏疾病的共同后果，持续的肝脏细胞损伤启动炎症反应，随后导致肝脏星状细胞和成纤维细胞激活。活性氧在肝脏损伤中发挥重要作用，也是治疗肝纤维化的重要靶点。据报道，氢水对活性氧相关疾病具有理想的治疗价值，本研究的目的是探讨氢气水对肝脏纤维化的作用，并尝试研究其作用机制。

C57BL/6小鼠分别喂养氢气水或对照水，采用四氯化碳、硫代乙酰胺和胆管结扎诱导肝脏纤维化。从小鼠肝脏分离除肝细胞和星形细胞，通过加入氢气培养基，观察体外培养的肝脏细胞和肝星形细胞产生活性氧的变化。

结果发现，小鼠喝氢气水可以显著抑制四氯化碳、硫代乙酰胺诱导的肝脏纤维化，但是对胆管结扎诱导的肝脏纤维化没有作用（这一报道和过去的报道不一致，需要进行深入分析和验证），氢气对体外培养的抗环霉素诱导的肝脏细胞羟自由基水平和细胞死亡有明显的抑制作用，但对抗环霉素诱导的星形细胞激活没有影响。

研究结果表明，氢气可以通过清除肝脏细胞内羟自由基治疗肝纤维化。

Effectsof Oral Intake of Hydrogen Water on Liver Fibrogenesis in Mice

Department of Surgery, Graduate Schoolof Medicine, Kyoto University, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto6068507, JapanAim

Liver fibrosis is the universal consequenceof chronic liver diseases. Sustained hepatocyte injury initiates aninflammatory response, thereby activating hepatic stellate cells, the principalfibrogenic cells in the liver. Reactive oxygen species are involved in liverinjury and are a promising target for the treating liver fibrosis. Hydrogenwater is reported to have potential as a therapeutic tool for the reactiveoxygen species-associated disorders. This study aimed to investigate theeffects of hydrogen water on liver fibrogenesis and the mechanisms underlyingthese effects.

Methods

C57BL/6 mice were fed with hydrogen wateror control water, and subjected to carbon tetrachloride, thioacetamide and bileduct ligation treatments to induce liver fibrosis. Hepatocytes and hepaticstellate cells were isolated from mice and cultured with or without hydrogen totest the effects of hydrogen on reactive oxygen species-induced hepatocyteinjuries or hepatic stellate cell activation.

Results

Oral intake of hydrogen water significantlysuppressed liver fibrogenesis in the carbon tetrachloride and thioacetamidemodels, but these effects were not seen in the bile duct ligation model.Treatment of isolated hepatocyte with 1 μg/mL antimycin A generated hydroxylradicals. Culturing in the hydrogen-rich medium selectively suppressed thegeneration of hydroxyl radicals in hepatocytes and significantly suppressedhepatocyte death induced by antimycin A; however, it did not suppress hepaticstellate cell activation.

Conclusions

we conclude that hydrogen water protectshepatocytes from injury by scavenging hydroxyl radicals and thereby suppressesliver fibrogenesis in mice.