NDLI: Hydrogen Sulfide Ameliorates Early Brain Injury Following Subarachnoid Hemorrhage in Rats

Content Provider	Springer Nature Link
Author	Cui, Yonghua Duan, Xiaochun Li, Haiying Dang, Baoqi Yin, Jia Wang, Yang Gao, Anju Yu, Zhengquan Chen, Gang
Copyright Year	2015
Abstract	Increasing studies have demonstrated the neuroprotective effect of hydrogen sulfide (H$_{2}$S) in central nervous system (CNS) diseases. However, the potential application value of H$_{2}$S in the therapy of subarachnoid hemorrhage (SAH) is still not well known. This study was to investigate the potential effect of H$_{2}$S on early brain injury (EBI) induced by SAH and explore the underlying mechanisms. The role of sodium hydrosulfide (NaHS), a donor of H$_{2}$S, in SAH-induced EBI, was investigated in both in vivo and in vitro. A prechiasmatic cistern single injection model was used to produce experimental SAH in vivo. In vitro, cultured primary rat cortical neurons and human umbilical vein endothelial cells (HUVECs) were exposed to OxyHb at concentration of 10 μM to mimic SAH. Endogenous production of H$_{2}$S in the brain was significantly inhibited by SAH. The protein levels of the predominant H$_{2}$S-generating enzymes in the brain, including cystathionineb-synthase (CBS) and 3-mercaptopyruvate sulfur transferase (3MST), were also correspondingly reduced by SAH, while treatment with NaHS restored H$_{2}$S production and the expressions of CBS and 3MST. More importantly, NaHS treatment could significantly attenuate EBI (including brain edema, blood–brain barrier disruption, brain cell apoptosis, inflammatory response, and cerebral vasospasm) after SAH. In vitro, H$_{2}$S protects neurons and endothelial function by functioning as an antioxidant and antiapoptotic mediator. Our results suggest that NaSH as an exogenous H$_{2}$S donor could significantly reduce EBI induced by SAH.
Starting Page	3646
Ending Page	3657
Page Count	12
File Format	PDF
ISSN	08937648
Journal	Molecular Neurobiology
Volume Number	53
Issue Number	6
e-ISSN	15591182
Language	English
Publisher	Springer US
Publisher Date	2015-06-26
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Subarachnoid hemorrhage Early brain injury Hydrogen sulfide Oxidative stress Inflammatory response Neurosciences Neurobiology Cell Biology Neurology
Content Type	Text
Resource Type	Article
Subject	Neurology Cellular and Molecular Neuroscience

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