Yong Wang
Guilin Medical University
48 Papers
33 Citations
Yong Wang is an academic researcher from Guilin Medical University. The author has contributed to research in topics: Medicine & Biology. The author has an hindex of 11, co-authored 21 publications.
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Papers
Formononetin mediates neuroprotection against cerebral ischemia/reperfusion in rats via downregulation of the Bax/Bcl-2 ratio and upregulation PI3K/Akt signaling pathway
TL;DR: It is found that formononetin has significantly reduced the infarcted volume and the brain water content, and improved the neurological deficit, and the molecular mechanisms may correlate with the downregulation of the Bax/Bcl-2 ratio and the activation of PI3K/Akt signaling pathway.
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Neuroprotective Mechanisms of Calycosin Against Focal Cerebral Ischemia and Reperfusion Injury in Rats.
TL;DR: The data reveal that calycosin exerts a neuroprotective effect on cerebral ischemia and reperfusion injury, and the mechanisms maybe associated with its anti-autophagic, anti-apoptotic and anti-inflammatory action.
Biochanin A Provides Neuroprotection Against Cerebral Ischemia/Reperfusion Injury by Nrf2-Mediated Inhibition of Oxidative Stress and Inflammation Signaling Pathway in Rats.
Minmin Guo,Huiling Lu,Qin Jian,Sheng-biao Qu,Wenbo Wang,Yanhong Guo,Weiyong Liao,Song Mengwei,Jian Chen,Yong Wang +9 more
TL;DR: The results indicated that biochanin A protected the brain against ischemic injury in rats by anti-oxidative and anti-inflammatory actions.
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Calycosin inhibits the in vitro and in vivo growth of breast cancer cells through WDR7-7-GPR30 Signaling
TL;DR: The possibility that calycosin inhibited the proliferation of breast cancer cells, at least partially, through WDR7-7-GPR30 signaling is suggested, which may explain why calyCosin can exert inhibitory effects on ER− breast cancer.
Biochanin A protects against focal cerebral ischemia/reperfusion in rats via inhibition of p38-mediated inflammatory responses.
TL;DR: Taken together, biochanin A has been shown to have neuroprotective effects in cerebral ischemia/reperfusion, and the mechanisms may correlate with inhibiting inflammatory response, as well as the inactivation of p38 signaling pathway.
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