HepG2細胞におけるCD36発現抑制を介した水素による脂肪酸取り込みおよび脂質蓄積の低減
This in vitro study examined the effects of molecular hydrogen on fatty acid metabolism in human HepG2 hepatoma cells challenged with a palmitate-BSA complex. Hydrogen pretreatment for 24 hours significantly reduced both fatty acid uptake and intracellular lipid accumulation, as measured by spectrofluorometry and Oil Red O staining, respectively. These changes were accompanied by suppressed JNK phosphorylation. Notably, while CD36 mRNA levels remained unchanged, CD36 protein expression was markedly decreased, indicating post-translational regulation as the operative mechanism. These findings provide molecular-level insight into how hydrogen modulates lipid metabolism in hepatic cells, with potential relevance to in vivo conditions involving lipid metabolic dysregulation.
Hydrogen suppresses JNK phosphorylation and reduces CD36 protein expression through post-translational regulation without altering CD36 mRNA levels, thereby decreasing fatty acid uptake and lipid accumulation in hepatic cells.
This is basic research at the cellular or molecular level. For human application, inhalation is the most promising delivery route, but inhalation carries explosion risk and concentration matters (empirical LFL of 10%; high-concentration devices are not recommended).
See also:
https://h2-papers.org/en/papers/23448206