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Hydrogen-rich water protects liver injury in nonalcoholic steatohepatitis though HO-1 enhancement via IL-10 and Sirt 1 signaling
American Journal of Physiology-Gastrointestinal and Liver Physiology ( IF 3.9 ) Pub Date : 2021-01-13 , DOI: 10.1152/ajpgi.00158.2020
Shao-Wei Li 1 , Terumi Takahara 2 , Weitao Que 3 , Masayuki Fujino 4 , Wen-zhi Guo 5 , Shin-ichi Hirano , Li-Ping Ye 1 , Xiao-Kang Li 3
Affiliation  

Nonalcoholic steatohepatitis (NASH) could progress to hepatic fibrosis when absence of effective control. The purpose of our experiment was to investigate the protective effect of drinking water with high concentration of hydrogen in our study named hydrogen rich water (HRW) on mice with non-alcoholic fatty liver disease to elucidate the mechanism underlying the molecular hydrogen therapeutic action. The choline-supplemented, L-amino acid-defined (CSAA) or choline-deficient, L-amino acid-defined (CDAA) diet for 20 weeks were used to induce NASH and fibrosis in the mice model and simultaneously treated with HRW for different periods of time. Primary hepatocytes were stimulated by palmitate in order to mimic a liver lipid metabolism during fatty liver formation. Mice in the CSAA + HRW group had lower serum levels of ALT and AST and milder histological damage. The inflammatory cytokines were expressed at lower levels in the HRW group than in the CSAA group. Importantly, HRW reversed hepatocyte apoptosis as well as hepatic inflammation and fibrosis in pre-existing hepatic fibrosis specimens. Molecular hydrogen inhibits the lipopolysaccharide-induced production of inflammation cytokines through an HO-1/IL-10-independent pathway. Furthermore, HRW improved hepatic steatosis in the CSAA + HRW group. Sirt1 induction by molecular hydrogen via the HO-1/AMPK/PPARα/PPARγ pathway suppresses palmitate-mediated abnormal fat metabolism. Orally administered HRW suppressed steatosis induced by CSAA and attenuated fibrosis induced by CDAA, possibly by reducing oxidative stress and the inflammation response.

中文翻译:

富氢水可通过IL-10和Sirt 1信号通路增强HO-1,从而保护非酒精性脂肪性肝炎的肝损伤

如果缺乏有效的控制,非酒精性脂肪性肝炎(NASH)可能会发展为肝纤维化。本实验的目的是研究高浓度氢饮用水对非酒精性脂肪肝小鼠的保护作用,以阐明分子氢治疗作用的机制。补充胆碱的L-氨基酸定义(CSAA)或胆碱缺乏的L-氨基酸定义(CDAA)饮食20周,以诱导小鼠模型中的NASH和纤维化,并同时用HRW处理不同的模型时间段。棕榈酸酯刺激原代肝细胞,以模拟脂肪肝形成过程中的肝脂质代谢。CSAA + HRW组的小鼠血清ALT和AST含量较低,组织学损伤较轻。与CSAA组相比,HRW组炎症细胞因子的表达水平较低。重要的是,HRW逆转了先前存在的肝纤维化标本中的肝细胞凋亡以及肝炎症和纤维化。分子氢通过HO-1 / IL-10-独立途径抑制脂多糖诱导的炎症细胞因子的产生。此外,在CSAA + HRW组,HRW改善了肝脂肪变性。分子氢通过HO-1 / AMPK /PPARα/PPARγ途径对Sirt1的诱导抑制了棕榈酸酯介导的异常脂肪代谢。口服HRW可能通过减少氧化应激和炎症反应来抑制CSAA诱导的脂肪变性和CDAA诱导的纤维化。与CSAA组相比,HRW组炎症细胞因子的表达水平较低。重要的是,HRW逆转了先前存在的肝纤维化标本中的肝细胞凋亡以及肝炎症和纤维化。分子氢通过HO-1 / IL-10-独立途径抑制脂多糖诱导的炎症细胞因子的产生。此外,在CSAA + HRW组,HRW改善了肝脂肪变性。分子氢通过HO-1 / AMPK /PPARα/PPARγ途径对Sirt1的诱导抑制了棕榈酸酯介导的异常脂肪代谢。口服HRW可能通过减少氧化应激和炎症反应来抑制CSAA诱导的脂肪变性和CDAA诱导的纤维化。与CSAA组相比,HRW组炎症细胞因子的表达水平较低。重要的是,HRW逆转了先前存在的肝纤维化标本中的肝细胞凋亡以及肝炎症和纤维化。分子氢通过HO-1 / IL-10-独立途径抑制脂多糖诱导的炎症细胞因子的产生。此外,在CSAA + HRW组,HRW改善了肝脂肪变性。分子氢通过HO-1 / AMPK /PPARα/PPARγ途径对Sirt1的诱导抑制了棕榈酸酯介导的异常脂肪代谢。口服HRW可能通过减少氧化应激和炎症反应来抑制CSAA诱导的脂肪变性和CDAA诱导的纤维化。HRW逆转了先前存在的肝纤维化标本中的肝细胞凋亡以及肝炎症和纤维化。分子氢通过HO-1 / IL-10-独立途径抑制脂多糖诱导的炎症细胞因子的产生。此外,在CSAA + HRW组,HRW改善了肝脂肪变性。分子氢通过HO-1 / AMPK /PPARα/PPARγ途径对Sirt1的诱导抑制了棕榈酸酯介导的异常脂肪代谢。口服HRW可能通过减少氧化应激和炎症反应来抑制CSAA诱导的脂肪变性和CDAA诱导的纤维化。HRW逆转了先前存在的肝纤维化标本中的肝细胞凋亡以及肝炎症和纤维化。分子氢通过HO-1 / IL-10-独立途径抑制脂多糖诱导的炎症细胞因子的产生。此外,在CSAA + HRW组,HRW改善了肝脂肪变性。分子氢通过HO-1 / AMPK /PPARα/PPARγ途径对Sirt1的诱导抑制了棕榈酸酯介导的异常脂肪代谢。口服HRW可能通过减少氧化应激和炎症反应来抑制CSAA诱导的脂肪变性和CDAA诱导的纤维化。分子氢通过HO-1 / IL-10-独立途径抑制脂多糖诱导的炎症细胞因子的产生。此外,在CSAA + HRW组,HRW改善了肝脂肪变性。分子氢通过HO-1 / AMPK /PPARα/PPARγ途径对Sirt1的诱导抑制了棕榈酸酯介导的异常脂肪代谢。口服HRW可能通过减少氧化应激和炎症反应来抑制CSAA诱导的脂肪变性和CDAA诱导的纤维化。分子氢通过HO-1 / IL-10-独立途径抑制脂多糖诱导的炎症细胞因子的产生。此外,在CSAA + HRW组,HRW改善了肝脂肪变性。分子氢通过HO-1 / AMPK /PPARα/PPARγ途径对Sirt1的诱导抑制了棕榈酸酯介导的异常脂肪代谢。口服HRW可能通过减少氧化应激和炎症反应来抑制CSAA诱导的脂肪变性和CDAA诱导的纤维化。
更新日期:2021-01-13
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