J
Junfeng Wu
Researcher at Fudan University
Publications - 10
Citations - 80
Junfeng Wu is an academic researcher from Fudan University. The author has contributed to research in topics: Internal medicine & Downregulation and upregulation. The author has an hindex of 5, co-authored 6 publications receiving 54 citations.
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Journal ArticleDOI
DHT Inhibits the Aβ25–35-Induced Apoptosis by Regulation of Seladin-1, Survivin, XIAP, bax, and bcl-xl Expression Through a Rapid PI3-K/Akt Signaling in C6 Glial Cell Lines
TL;DR: DHT inhibits Aβ25–35-induced apoptosis by a rapid nongenic PI-3K/Akt activation as well as regulation of seladin-1, survivin, XIAP, bcl-xl, and bax proteins.
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Testosterone up-regulates seladin-1 expression by iAR and PI3-K/Akt signaling pathway in C6 cells.
TL;DR: It is suggested that testosterone regulated the expression of seladin-1 by the intracellular androgen receptor (iAR)-mediated genomic signaling pathway and the non-genomic PI3-K/Akt signaling pathway in C6 glial cells.
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Function of Thymosin Beta-4 in Ethanol- Induced Microglial Activation
TL;DR: This study is the first to demonstrate the function of Tβ4 in ethanol-induced microglia activation, thus contributing to a more robust understanding of the role of T β4 treatment in CNS disease.
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Anti‐inflammatory effects of doxepin hydrochloride against LPS‐induced C6‐glioma cell inflammatory reaction by PI3K‐mediated Akt signaling
TL;DR: It is demonstrated that doxepin was able to suppress these effects induced by LPS, through activation of the phosphatidylinositol‐3‐kinase‐mediated protein kinase B (Akt) pathway, which highlights the potential role of doxEPin against neuroinflammatory‐related disease in the brain.
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Protective Effect of DHT on Apoptosis Induced by U18666A via PI3K/Akt Signaling Pathway in C6 Glial Cell Lines.
TL;DR: DHT may inhibit U18666A-induced apoptosis by regulating downstream apoptosis-related proteins including seladin-1, caspase-3, Bcl-xL, and Bax through activation of the PI3K/Akt signal pathway.