Area of research
Neurology · Developmental Neuroscience
Research interest
Research interests include Neuroinflammation and Neurodegeneration Mechanisms, Neurogenesis and neuroplasticity mechanisms, Barrier Structure and Function Studies, and Neurological Disease Mechanisms and Treatments.
Neuroglia and immune cells play different roles in neuroinflammation and neuroimmune response in post-stroke neural injury and repair
Targeting angiogenesis and white matter repair for enhanced functional recovery after acute ischemic stroke: A focus on the roles of glial cells
Chronic but not acute nicotine treatment ameliorates acute inflammation‐induced working memory impairment by increasing <scp>CRTC1</scp> and <scp>HCN2</scp> in adult male mice
Nicotine’s effect on cognition, a friend or foe?
CRTC1 is a potential target to delay aging-induced cognitive deficit by protecting the integrity of the blood-brain barrier via inhibiting inflammation
Clemastine attenuates AD-like pathology in an AD model mouse via enhancing mTOR-mediated autophagy
Acute Nicotine Treatment Alleviates LPS-Induced Impairment of Fear Memory Reconsolidation Through AMPK Activation and CRTC1 Upregulation in Hippocampus
<scp>STAT</scp> 4 activation by leukemia inhibitory factor confers a therapeutic effect on intestinal inflammation
Inhibition of Reactive Astrocytes with Fluorocitrate Ameliorates Learning and Memory Impairment Through Upregulating CRTC1 and Synaptophysin in Ischemic Stroke Rats
NG2-glia cell proliferation and differentiation by glial growth factor 2 (GGF2), a strategy to promote functional recovery after ischemic stroke
Melatonin alleviates lipopolysaccharide-compromised integrity of blood-brain barrier through activating AMP-activated protein kinase in old mice
β2-Adrenergic Receptor-Mediated HIF-1α Upregulation Mediates Blood Brain Barrier Damage in Acute Cerebral Ischemia
Corrigendum: β2-Adrenergic Receptor-Mediated HIF-1α Upregulation Mediates Blood Brain Barrier Damage in Acute Cerebral Ischemia
Chronic N-acetylcysteine treatment alleviates acute lipopolysaccharide-induced working memory deficit through upregulating caveolin-1 and synaptophysin in mice
Normobaric Hyperoxia Extends Neuro- and Vaso-Protection of N-Acetylcysteine in Transient Focal Ischemia