Concomitant inhibition of oxidative stress and angiogenesis by chronic hydrogen-rich saline and N-acetylcysteine treatments improves systemic, splanchnic and hepatic hemodynamics of cirrhotic rats.
Pei-Chang Lee, Ying-Ying Yang, Chien-Sheng Huang, Shie-Liang Hsieh, Kuei-Chuan Lee, Yun-Cheng Hsieh, Tzung-Yan Lee, Han-Chieh Lin · Hepatology research : the official journal of the Japan Society of Hepatology · 2015
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Independent study record
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H2HUBB TAKEAWAY
In a laboratory model, the data indicate that 1-month treatment of N-acetylcysteine or hydrogen-rich saline significantly ameliorated systemic and splanchnic hyperdynamic circulation, corrected hepatic endothelial dysfunction, and decreased intrahepatic resistance and mesenteric angiogenesis by inhibiting inflammatory cytokines, nitric oxide, VEGF and reducing mesenteric oxidative stress in cirrhotic rats. The authors concluded that n-Acetylcysteine and the new antioxidant, hydrogen-rich saline are potential treatments for the complications of cirrhosis. These findings come from a laboratory model and suggest molecular hydrogen's biological potential. Further research is needed to determine clinical relevance.
What the Researchers Tested
Like N-acetylcysteine, hydrogen-rich saline is a new documented antioxidant with the potential to treat the complications of liver diseases.
How Molecular Hydrogen Was Used
In this study, hemodynamics, splanchnic angiogenesis and hepatic endothelial dysfunction were measured in common bile duct ligation (BDL)-cirrhotic rats receiving 1-month treatment of vehicle, N-acetylcysteine and hydrogen-rich saline immediately after BDL. Additionally, acute effects of N-acetylcysteine and hydrogen-rich saline on vascular endothelial growth factor (VEGF)-induced tubule formation and migration of human umbilical vein endothelial cells (HUVEC) were also evaluated.
What Molecular Hydrogen Changed
The data indicate that 1-month treatment of N-acetylcysteine or hydrogen-rich saline significantly ameliorated systemic and splanchnic hyperdynamic circulation, corrected hepatic endothelial dysfunction, and decreased intrahepatic resistance and mesenteric angiogenesis by inhibiting inflammatory cytokines, nitric oxide, VEGF and reducing mesenteric oxidative stress in cirrhotic rats.
Proposed Mechanism
The data indicate that 1-month treatment of N-acetylcysteine or hydrogen-rich saline significantly ameliorated systemic and splanchnic hyperdynamic circulation, corrected hepatic endothelial dysfunction, and decreased intrahepatic resistance and mesenteric angiogenesis by inhibiting inflammatory cytokines, nitric oxide, VEGF and reducing mesenteric oxidative stress in cirrhotic rats. In vivo studies revealed that acute co-incubation of N-acetylcysteine or hydrogen-rich saline with VEGF effectively suppressed VEGF-induced angiogenesis and migration of HUVEC accompanied by decreasing of oxidative stress and inflammatory cytokines. The data indicate that 1-month treatment of N-acetylcysteine or hydrogen-rich saline significantly ameliorated systemic and splanchnic hyperdynamic circulation, corrected hepatic endothelial dysfunction, and decreased intrahepatic resistance and mesenteric angiogenesis by inhibiting inflammatory cytokines, nitric oxide, VEGF and reducing mesenteric oxidative stress in cirrhotic rats.
Authors’ Conclusion
These findings come from a laboratory model and suggest molecular hydrogen's biological potential. Further research is needed to determine clinical relevance.