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Jie Fang

Publications -  7
Citations -  351

Jie Fang is an academic researcher. The author has contributed to research in topics: Neuroprotection & Reactive oxygen species. The author has an hindex of 7, co-authored 7 publications receiving 300 citations.

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Enhanced Therapeutic Potential of Nano-Curcumin Against Subarachnoid Hemorrhage-Induced Blood-Brain Barrier Disruption Through Inhibition of Inflammatory Response and Oxidative Stress.

TL;DR: The results indicated that Cur-NPs showed enhanced therapeutic effects than that of curcumin in improving neurological function, reducing brain water content, and Evans blue dye extravasation after SAH, and revealed that the strategy of using Cur- NPs could be a promising way in improved neurological function in EBI after experimental rat SAH.
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Carnosine Attenuates Brain Oxidative Stress and Apoptosis After Intracerebral Hemorrhage in Rats.

TL;DR: The results indicate that intraperitoneal administration of Carnosine significantly attenuates brain edema, blood–brain barrier disruption, oxidative stress, microglia activation and neuronal apoptosis of perihematoma at 72 h following ICH in rats models, and suggest that Carno may provide neuroprotective effect after experimental ICH.
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Activation of mGluR5 Attenuates Microglial Activation and Neuronal Apoptosis in Early Brain Injury After Experimental Subarachnoid Hemorrhage in Rats

TL;DR: It is found that selective mGluR5 orthosteric agonist CHPG or positive allosteric modulator VU0360172 administration significantly improves neurological function and attenuates brain edema in EBI after SAH.
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Carnosine Attenuates Early Brain Injury Through Its Antioxidative and Anti-apoptotic Effects in a Rat Experimental Subarachnoid Hemorrhage Model

TL;DR: It is found that intraperitoneal administration of carnosine improved neurobehavioral deficits, attenuated brain edema and blood–brain barrier permeability, and decreased reactive oxygen species level at 48 h following SAH in rat models, indicating that administration of Carnosine may provide neuroprotection in EBI followingSAH in rats.
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DSePA Antagonizes High Glucose-Induced Neurotoxicity: Evidences for DNA Damage-Mediated p53 Phosphorylation and MAPKs and AKT Pathways

TL;DR: The results suggested that high glucose showed significant cytotoxicity through launching mitochondria-mediated apoptosis in PC12 cells, accompanied by poly (ADP-ribose) polymerase (PARP) cleavage, caspase activation, and mitochondrial dysfunction, but 3,3′-diselenodipropionic acid (DSePA), a derivative of selenocystine, demonstrated its protective effect against high glucose-induced neurotoxicity.