Jia-Yong Wu
Nanjing Medical University
5 Papers
Jia-Yong Wu is an academic researcher from Nanjing Medical University. The author has contributed to research in topics: ATP-sensitive potassium channel & Channel blocker. The author has an hindex of 4, co-authored 4 publications.
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Papers
Iptakalim Alleviates Rotenone-Induced Degeneration of Dopaminergic Neurons through Inhibiting Microglia-Mediated Neuroinflammation
TL;DR: It is demonstrated that systematic administration with iptakalim (IPT), an adenosine triphosphate (ATP) opener, could alleviate rotenone-induced degeneration of dopaminergic neurons in rat substantia nigra along with the downregulation of microglial activation and mRNA levels of tumor necrosis factor-α (TNF-α) and cyclooxygenase-2 (COX-2).
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Opening of microglial K(ATP) channels inhibits rotenone-induced neuroinflammation.
TL;DR: It is demonstrated that rat primary cultured MG expressed Kir6.1 and SUR2 subunits of KATP channel, which was identical to that expressed in BV‐2 microglial cell line, and diazoxide exhibited neuroprotective effects against rotenone along with the inhibition of microglia activation and neuroinflammation.
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The regulation of rotenone-induced inflammatory factor production by ATP-sensitive potassium channel expressed in BV-2 cells.
TL;DR: Activation of K(ATP) channel might be a new therapeutic strategy for treating neuroinflammatory and neurodegenerative disorders.
Identification of D359-0396 as a novel inhibitor of the activation of NLRP3 inflammasome
Zihao Li,Senlin Ji,Chuyu Wu,Jia-Yong Wu,Runjing Cao,Yunshu Wang,Yun Xu,Jingwei Li,Cun-Jin Zhang +8 more
TL;DR: In this paper , the anti-pyroptosis and anti-inflammation effect of D359-0396 has been evaluated in both mouse and human macrophages using more than 20,000 small molecules and found that the drug is well-tolerant without remarkable disruption of homeostasis.
Activation of Group II/III metabotropic glutamate receptors attenuates LPS-induced astroglial neurotoxicity via promoting glutamate uptake.
TL;DR: It is found that the repression of astroglial uptake function could be revived by GSH, and both Group II and III mGluR agonists could recover the endogenous reduced glutathione (GSH) level in LPS‐treated astrocytes, suggesting that the possible mechanisms of neuroprotection by either Type II or Type III mgluR activation may involve restoration of endogenous GSH.