Molecular Hydrogen Attenuated N-methyl-N-Nitrosourea Induced Corneal Endothelial Injury by Upregulating Anti-Apoptotic Pathway.
Runpu Li, Yingxin Qu, Xiaoqi Li, Ye Tao, Qinghua Yang, Junyi Wang, Yumei Diao, Qian Li, Yifan Fang, Yifei Huang, Liqiang Wang · Investigative ophthalmology & visual science · 2021
Research-use notice
Independent study record
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H2HUBB TAKEAWAY
It was shown that MNU could inhibit the proliferation and specific physiological functions of CECs by increasing apoptosis and decreasing the expression of ZO-1 and Na+/K+-ATPase, whereas H₂ improved the proliferation and physiological function of CECs by anti-apoptosis. This source-grounded publication contributes evidence relevant to molecular hydrogen and is retained in a transparent general research category when a more specific study design is not supported by the indexed record.
What the Publication Examined
The aim of this study was to investigate the effect of molecular hydrogen (H₂) on MNU-induced corneal endothelial cell (CEC) injury and the underlying mechanism.
How Molecular Hydrogen Was Addressed
MNU-induced animal models of CEC injury were washed with hydrogen-rich saline (HRS) for 14 days. The effect of H₂ was examined using morphological and functional assays.
What the Publication Reported
It was shown that MNU could inhibit the proliferation and specific physiological functions of CECs by increasing apoptosis and decreasing the expression of ZO-1 and Na+/K+-ATPase, whereas H₂ improved the proliferation and physiological function of CECs by anti-apoptosis.