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Hydrogen inhalation therapy regulates lactic acid metabolism following subarachnoid hemorrhage through the HIF-1α pathway.

Authors :
Peng, Zheng
Li, Xiao-Jian
Pang, Cong
Zhang, Jia-Tong
Zhu, Qi
Sun, Jia-Qing
Wang, Juan
Cao, Bo-Qiang
Zhang, Yu-Hua
Lu, Yue
Li, Wei
Hang, Chun-Hua
Zhuang, Zong
Source :
Biochemical & Biophysical Research Communications. Jun2023, Vol. 663, p192-201. 10p.
Publication Year :
2023

Abstract

The neuroprotective effects of hydrogen have been demonstrated, but the mechanism is still poorly understood. In a clinical trial of inhaled hydrogen in patients with subarachnoid hemorrhage (SAH), we found that hydrogen reduced the accumulation of lactic acid in the nervous system. There are no studies demonstrating the regulatory effect of hydrogen on lactate and in this study we hope to further clarify the mechanism by which hydrogen regulates lactate metabolism. In cell experiments, PCR and Western Blot showed that HIF-1α was the target related to lactic acid metabolism that changed the most before and after hydrogen intervention. HIF-1α levels were suppressed by hydrogen intervention treatment. Activation of HIF-1α inhibited the lactic acid-lowering effect of hydrogen. We have also demonstrated the lactic acid-lowering effect of hydrogen in animal studies. Our work clarifies that hydrogen can regulate lactate metabolism via the HIF-1αpathway, providing new insights into the neuroprotective mechanisms of hydrogen. • In clinical trials, hydrogen therapy reduced cerebrospinal fluid lactate levels in patients with subarachnoid hemorrhage. • HIF-1α is the target associated with the greatest change in lactate metabolism before and after hydrogen intervention. • Hydrogen regulates lactate metabolism after SAH via the HIF-1α pathway. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
0006291X
Volume :
663
Database :
Academic Search Index
Journal :
Biochemical & Biophysical Research Communications
Publication Type :
Academic Journal
Accession number :
163694784
Full Text :
https://doi.org/10.1016/j.bbrc.2023.04.072