Shuo Chen
Anhui Medical University
5 Papers
Shuo Chen is an academic researcher from Anhui Medical University. The author has contributed to research in topics: Chemistry & Vasodilation. The author has an hindex of 3, co-authored 3 publications.
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Papers
Role of CSE-Produced H2S on Cerebrovascular Relaxation via RhoA-ROCK Inhibition and Cerebral Ischemia-Reperfusion Injury in Mice.
TL;DR: The findings revealed that the CSE-produced H2S induced cerebrovascular relaxation is generated from endothelial cells and the mechanism of vascular relaxation may relate to inhibition of RhoA-ROCK pathway.
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Involvement of Hydrogen Sulfide in Endothelium-Derived Relaxing Factor-Mediated Responses in Rat Cerebral Arteries.
TL;DR: EDHF-mediated responses in rat cerebral arteries were due to HS activating the KCa
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VEGFR2 in vascular smooth muscle cells mediates H2S-induced dilation of the rat cerebral basilar artery.
TL;DR: In this article , the authors investigated whether the VEGFR2 mediates hydrogen sulfide (H2S)-induced relaxation of the rat cerebral vasculature and found that H2S donor NaHS induced significant relaxation of cerebral basilar artery (CBA) and vascular smooth muscle cells (VSMCs).
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Total Flavones of Rhododendron simsii Planch Flower Protect against Cerebral Ischemia-Reperfusion Injury via the Mechanism of Cystathionine-γ-Lyase-Produced H2S.
Shuo Chen,Jian-Hua Zhang,Jian-Hua Zhang,You-Yang Hu,Dong-Hua Hu,Shan-Shan Gao,Yi-Fei Fan,Yu-Ling Wang,Yi Jiao,Zhi-Wu Chen +9 more
TL;DR: The data indicate that TFR has a protective effect against the cerebral ischemia-reperfusion injury via CSE-produced H2S and endothelial NO and/or PGI2 to relax the cerebral artery.
Roles of the RhoA-ROCK Signaling Pathway in the Endothelial H2S Production and Vasodilation in Rat Cerebral Arteries
TL;DR: The results demonstrated that endothelial H2S production is promoted by activation of the M receptor but inhibited by the RhoA-ROCK pathway in rat cerebral arteries; the endothelialH2S induces cerebral vasodilation by inhibiting this pathway to reduce phosphorylation of MLC and [Ca2+]i in vascular smooth muscle cells.
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