A5101795878- Neuroinflammation and Neurodegeneration Mechanisms
- Tryptophan and brain disorders
- Circadian rhythm and melatonin
- Ocular Surface and Contact Lens
- Phytochemistry and Bioactive Compounds
- Sphingolipid Metabolism and Signaling
- Advanced Glycation End Products research
- Inflammasome and immune disorders
- Stroke Rehabilitation and Recovery
- Olfactory and Sensory Function Studies
- Stress Responses and Cortisol
- Menopause: Health Impacts and Treatments
- Fungal Biology and Applications
- Corneal Surgery and Treatments
- Alkaloids: synthesis and pharmacology
- interferon and immune responses
- Phytochemistry and Biological Activities
- Herpesvirus Infections and Treatments
- Neurological Disease Mechanisms and Treatments
- Toxoplasma gondii Research Studies
- Phytochemistry and Bioactivity Studies
Affiliated Eye Hospital of Wenzhou Medical College
2022-2024
Wenzhou Medical University
2022-2024
Xinxiang Central Hospital
2024
First Affiliated Hospital of Xinxiang Medical University
2023
Nanjing University of Chinese Medicine
2023
Henan Polytechnic University
2023
China Pharmaceutical University
2008-2009
Abstract A significant decrease in estrogen levels puts menopausal women at high risk for major depression, which remains difficult to cure despite its relatively clear etiology. With the discovery of abnormally elevated inflammation depressed women, immune imbalance has become a novel focus study depression. In this paper, we examined characteristics and possible mechanisms caused by decreased during menopause found that deficiency disrupted homeostasis, especially inflammatory cytokines...
Stroke, especially ischemic stroke, is an important cause of neurological morbidity and mortality worldwide. Growing evidence suggests that the immune system plays intricate function in pathophysiology stroke. Gelsevirine (Gs), alkaloid from Gelsemium elegans, has been proven to decrease inflammation neuralgia osteoarthritis previously, but its role stroke unknown. In this study, middle cerebral artery occlusion (MCAO) mice model was used evaluate protective effect Gs on administration...
To assess the role of mitochondrial morphology and adenosine monophosphate-activated protein kinase (AMPK)/mitochondrial fission factor (MFF) in dry eye underlying mechanisms.
The cGAS-STING pathway has been shown to be an important mediator of inflammation. There is emerging evidence the importance this signaling cascade in a variety inflammatory diseases settings. Here, we present that mitochondrial DNA (mtDNA) damage-mediated plays role induction inflammation environmental dry eye (DE).
Abstract Multiple sclerosis (MS) is a chronic disease that characterized by demyelination and neuronal damage. Experimental autoimmune encephalomyelitis (EAE) mice are used to model the progression of MS mirror MS-like pathology. Previous researches have confirmed inhibition NLRP3 inflammasome significantly alleviated severity EAE spinal cord, but its effect on damage oligodendrocyte loss in brain remains unclear. In this study, female C57BL/6 were immunized with MOG35–55 PTX establish...
Purpose To explore whether circadian clock genes contribute to elicit inflammation in experimental dry eye (EDE).Methods RNA sequencing analyzed mRNA expression patterns EDE model. RT-qPCR and/or Western blot determined the of inflammatory factors and during EDE. MethylTarget™ assays promoter methylation levels Per vivo. Per2 or Per3 knockdown assessed their effects on vitro.Results We utilized an intelligently controlled environmental system (ICES) establish a mouse The significant...
Abstract Post-stroke depression (PSD) has more than 1/3 complications in ischemic stroke (IS) patients, but there is still no specific drug that can effectively prevent the occurrence of PSD. Cilostazol, commonly used treatment IS, been found to rescue cognition impairment recent years, whether it efficacy preventing PSD remains uncertain. In this study, a total 431 acute (AIS) patients treated with and without cilostazol during 2021-2022 were recruited followed up for 6 months. At end...