A5101756191- Neurological Disease Mechanisms and Treatments
- Alzheimer's disease research and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Neurological Disorders and Treatments
- Neuroscience and Neuropharmacology Research
- Traditional Chinese Medicine Analysis
- Natural product bioactivities and synthesis
- Cerebrovascular and Carotid Artery Diseases
- Intracerebral and Subarachnoid Hemorrhage Research
- Cholinesterase and Neurodegenerative Diseases
- Mitochondrial Function and Pathology
- Computational Drug Discovery Methods
- Amyotrophic Lateral Sclerosis Research
- Traumatic Brain Injury and Neurovascular Disturbances
- Genomics, phytochemicals, and oxidative stress
- Cytokine Signaling Pathways and Interactions
- Nuclear Receptors and Signaling
- IL-33, ST2, and ILC Pathways
- Natural Compound Pharmacology Studies
- Flavonoids in Medical Research
- Barrier Structure and Function Studies
- Psoriasis: Treatment and Pathogenesis
- NF-κB Signaling Pathways
- Bioactive natural compounds
- S100 Proteins and Annexins
Chinese Academy of Medical Sciences & Peking Union Medical College
2016-2025
Hunan Provincial Maternal and Child Health Hospital
2025
University of Leeds
2024
Peking Union Medical College Hospital
2019-2022
Sun Yat-sen Memorial Hospital
2012-2021
Sun Yat-sen University
2004-2021
Xinjiang Institute of Materia Medica
2019
Hebei Agricultural University
2013
Indiana University School of Medicine
2012
Indiana University – Purdue University Indianapolis
2012
The current development of immunotherapy for Alzheimer's disease is based on the assumption that human-derived amyloid beta protein (Abeta) can be targeted in a similar manner to animal cell-derived or synthetic Abeta. Because structure Abeta depends its source and presence cofactors, it great interest determine whether oligomeric species impair brain function and, if so, not their disruptive effects prevented using antibodies. We report untreated ex vivo human CSF contains dimers rapidly...
Complement factor C3 is the central component of complement system and a key inflammatory protein activated in Alzheimer9s disease (AD). Previous studies demonstrated that inhibition by overexpression soluble receptor-related y an AD mouse model led to reduced microgliosis, increased amyloid β (Aβ) plaque burden, neurodegeneration. To further address role pathology, we generated C3-deficient precursor (APP) transgenic (<i>APP;C3</i><sup>−/−</sup>). Brains were analyzed at 8, 12, 17 months...
Alzheimer9s disease (AD) is an age-related, progressive neurodegenerative disorder that occurs gradually and results in memory, behavior, personality changes. l-3-<i>n</i>-butylphthalide (l-NBP), extract from seeds of <i>Apium graveolens Linn</i> (Chinese celery), has been demonstrated to have neuroprotective effects on ischemic, vascular dementia, amyloid-β (Aβ)-infused animal models. In the current study, we examined l-NBP learning memory a triple-transgenic AD mouse model (3xTg-AD)...
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease affecting both upper and lower motor neurons (MNs) with large unmet medical needs. Multiple pathological mechanisms are considered to contribute the progression of ALS, including neuronal oxidative stress mitochondrial dysfunction. Honokiol (HNK) has been reported exert therapeutic effects in several neurologic models ischemia stroke, Alzheimer's Parkinson's disease. Here we found that honokiol also exhibited...
This study investigated whether anticerebral ischemia new drug, l-3-n-butylphthalide (l-NBP), improved behavioral recovery and enhanced hippocampal neurogenesis after cerebral in rats.The middle artery of rats was blocked for 2 h. The daily oral administrations 30 mg/kg l-NBP or vehicle were begun from the second day until sacrificed. L-NBP treatment markedly increased 5-bromo-2'-deoxyuridine (BrdU)-positive cells dentate gyrus (DG) injured hemisphere on 28 ischemia. amount newborn newly...
Blood–brain barrier (BBB) breakdown and the associated microvascular hyperpermeability are hallmark features of several neurological disorders, including traumatic brain injury (TBI). However, there is no viable therapeutic strategy to rescue BBB function. Tissue inhibitor metalloproteinase-1 (TIMP1) has been considered be beneficial for vascular integrity, but molecular mechanisms underlying functions TIMP1 remain elusive. Here, we report that executes a protective role on neuroprotective...
Abstract DL-3-n-butylphthalide (NBP) is a therapeutic drug used for ischemic stroke treatment. Here, we investigated the impact of NBP on development rat diabetic cataract induced by intraperitoneal injection streptozotocin (STZ). was then administrated oral gavage nine weeks. Cataract monitored through ophthalmoscope inspections. The levels blood glucose and serum reactive oxygen species (ROS), malondialdehyde (MDA) 8-Hydroxydeovexyguanosine (8-OHdG) were measured. Total soluble protein...
3-<i>n</i>-Butylphthalide (NBP) may be beneficial for the treatment of ischemic stroke with multiple actions on different pathophysiological processes. In present study, we investigated effect NBP isomers learning and memory impairment induced by chronic cerebral hypoperfusion in rats. Male Wistar rats were orally administered 10 30 mg/kg <i>l</i>-, <i>d</i>-, or <i>dl</i>-NBP daily 23 days after bilateral permanent occlusion common carotid arteries. Rats receiving <i>l</i>-NBP performed...
L-3-n-butylphthalide (L-NBP), an extract from seeds of Apium graveolens Linn (Chinese celery), has been shown to have neuroprotective effects on cerebral ischemic, vascular dementia and amyloid-β (Aβ)-induced animal models by inhibiting oxidative injury, neuronal apoptosis glial activation, regulating protein precursor (AβPP) processing reducing Aβ generation. The aim the present study was examine effect L-NBP learning memory in AβPP presenilin 1 (PS1) double-transgenic AD mouse model...
Our previous studies showed that L-3-n-butylphthalide (L-NBP), an extract from seeds of Apium graveolens Linn (Chinese celery), improved cognitive ability in animal models cerebral ischemia, vascular dementia, and Alzheimer's disease (AD). It is well known deficit AD caused by synaptic dysfunction. In this study, we investigated the effect L-NBP on hippocampal function APP/PS1 transgenic mice related mechanisms.Eighteen-month-old (Tg) were administrated 15 mg/kg oral gavage for 3 months....
Blood–brain barrier (BBB) disruption is a serious pathological consequence of traumatic brain injury (TBI), for which there are limited therapeutic strategies. Tissue inhibitor metalloproteinase-2 (TIMP2), molecule with dual functions inhibiting matrix metalloproteinase (MMP) activity and displaying cytokine-like through receptor binding, has been reported to inhibit VEGF-induced vascular hyperpermeability. Here, we investigate the ability TIMP2 ameliorate BBB in TBI underlying molecular...
We sought to investigate the anti-severe acute respiratory syndrome (SARS)-associated coronavirus (SCoV) activities of type I (alpha and beta) II (gamma) interferons (IFN) in vitro. Type IFNs protected cells from cytopathic effects (CPE) induced by SCoV, inhibited viral genomic RNA replication FRhk-4 (measured quantitative RT-PCR) a dose-dependent manner. Intracellular copies were reduced 50% IFN-alpha at concentration 25 U/ml IFN-beta 14 U/ml. IFN-gamma had fewer on inhibition infection...
3-n-butylphthalide (NBP) is a potentially beneficial drug for the treatment of ischemic stroke with multiple actions on different pathophysiological processes. In present study, effect l-, d-, and dl-NBP was investigated ADP-, collagen-, AA-induced platelet aggregation. l-NBP most potent among dl-NBP. At higher concentration aggregation greater than that l- or d-NBP alone. The ex vivo antiaggregatory activity 100mg/kg declined gradually after 2 hours, but considerable antiplatelet still...
The aim of this study was to investigate potential biomarkers Alzheimer's disease (AD). Changes in protein expression brain tissues from AβPP/PS1 transgenic mice were evaluated using two-dimensional gel electrophoresis combined with LC-MS/MS. A
AbstractAlzheimer's disease (AD) is a progressive neurodegenerative disease. Amyloid-β protein (Aβ), the hallmark of AD, invokes cascade mitochondrial dysfunction and eventually leads to neuronal death. l-3-n-Butylphthalide (l-NBP) has shown potent neuroprotective effects in stroke AD animal models. The present study evaluate effect l-NBP on Aβ25–35-induced injury possible mechanism human neuroblastoma SH-SY5Y cells. Our results showed that significantly attenuated cell death reduced...