A5057578690- Cell death mechanisms and regulation
- Immune Response and Inflammation
- Fungal Infections and Studies
- Airway Management and Intubation Techniques
- Pancreatic function and diabetes
- Tracheal and airway disorders
- NF-κB Signaling Pathways
- Immunotherapy and Immune Responses
- Pancreatitis Pathology and Treatment
- Inflammasome and immune disorders
- Anesthesia and Pain Management
- Pain Mechanisms and Treatments
- Cardiac, Anesthesia and Surgical Outcomes
- interferon and immune responses
- Forensic and Genetic Research
- Phytochemical Studies and Bioactivities
- RNA Interference and Gene Delivery
- Myasthenia Gravis and Thymoma
- Ginseng Biological Effects and Applications
- Ureteral procedures and complications
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Healthcare Decision-Making and Restraints
- Shoulder Injury and Treatment
- Peripheral Neuropathies and Disorders
- Trace Elements in Health
Chinese PLA General Hospital
2019-2022
Shanghai Institutes for Biological Sciences
2016-2017
University of Chinese Academy of Sciences
2016-2017
Second Military Medical University
1998-2017
Changhai Hospital
1998-2017
Chinese Academy of Sciences
2016-2017
Ministry of Public Security of the People's Republic of China
2013
Xiangya Hospital Central South University
2009
Central South University
2009
University of Michigan
2004
Sepsis-associated encephalopathy (SAE) is characterized as brain dysfunction associated with sepsis. In this study we sought to investigate the effects of resveratrol in mice SAE, well its NLRP3 inflammasome and IL-1β, which were critical pathogenesis SAE. SAE was induced via cecal ligation puncture (CLP), administered at two doses after surgery. Spatial learning memory functions evaluated by Morris water maze testing. Apoptosis hippocampus quantified using TUNEL assay. Inflammation...
MLKL, a key component downstream of RIPK3, is suggested to be terminal executor necroptosis. Genetic studies have revealed that Ripk3 ablation rescues embryonic lethality in Fadd- or Caspase-8-deficient mice. Given RIPK3 has also been implicated non-necroptotic pathways including apoptosis and inflammatory signaling, it remains unclear whether the Fadd(-/-) mice indeed caused by necropotosis. Here, we show genetic deletion Mlkl developmental defect Fadd-deficient Fadd(-/-)Mlkl(-/-) are...
RIPK3 mediates cell death and regulates inflammatory responses. Although genetic studies have suggested that RIPK3-MLKL-mediated necroptosis leads to embryonic lethality in Fadd or Caspase-8-deficient mice, the exact mechanisms are not fully understood. Here, we generated Ripk3 mutant mice by altering kinase domain (Ripk3Δ/Δ mice), thus abolishing its activity. Ripk3Δ/Δ cells were resistant stimulation vitro, protected from necroptotic diseases. mutation rescued Fadd−/− embryos, died within...
Abstract In mammalian cells, signaling pathways triggered by TNF can be switched from NF-κB activation to apoptosis and/or necroptosis. The in vivo mechanisms underlying the mutual regulation of these three are poorly understood. this article, we report that embryonic lethality RelA-deficient mice is partially prevented deletion Rip3 or Mlkl, but it fully rescued combined ablation Fadd and Mlkl blocking RIP1 kinase activity (RIP1K45A). RelA−/−Fadd−/−Rip3−/− triple-knockout (TKO)...
Tumor necrosis factor alpha (TNF-α) plays a critical role in the control of cryptococcal infection, and its insufficiency promotes persistence. To explore therapeutic potential TNF-α supplementation as booster host anti-cryptococcal responses, we engineered C. neoformans strain expressing murine TNF-α. Using model pulmonary cryptococcosis, demonstrated that TNF-α-producing enhances protective elements response including preferential T-cell accumulation improved Th1/Th2 cytokine balance,...
Summary Introduction Fungal transversal across the brain microvascular endothelial cells ( BMEC s) is essential step for development of cryptococcal meningoencephalitis. Annexin A2 (AnxA2) an important signaling protein involved in several intracellular processes such as membrane trafficking, endocytosis, and exocytosis. Aim To investigate roles mechanism AnxA2 during s. Results Cryptococcus neoformans infection initiated upregulation mouse Blockade with anti‐AnxA2 antibody led to a...
Inflammation is a response of body tissues to injury and infection. Compounds that can inhibit inflammation have been shown potential therapeutic clinical application. Gambogenic acid (GEA) has potent antitumor anti-inflammatory activities. Herein, the molecular mechanisms GEA's effect were investigated in lipopolysaccharide (LPS)-stimulated macrophage cells. The results showed pretreatment with GEA could markedly interleukin (IL)-1α, IL-1β, tumor necrosis factor-α, IFN-β, IL-12b, IL-23a...
Fas-associated death domain (FADD) and receptor-interacting serine/threonine kinase 3 (RIPK3) are multifunctional regulators of cell immune response. Using a mouse model cryptococcal infection, the roles FADD RIPK3 in anti-cryptococcal defense were investigated. Deletion alone led to increased inflammatory cytokine production C. neoformans-infected lungs, but combination with deletion it robust Th1-biased responses M1-biased macrophage activation. Rather than being protective, these...
BACKGROUND:Glutamate (GLU) is the most excitatory amino acid in central nervous system and plays an important role maintaining normal function of system. During cerebral ischemia, massive release GLU leads to neuronal necrosis apoptosis. It has been reported that dexmedetomidine (DEX) possesses anti-oxidant anti-apoptotic properties. The objective this study was investigate effects DEX on GLU-induced neurotoxicity PC12 cells. MATERIAL AND METHODS:PC12 cells were treated with 20 mM establish...
Abstract Caspase-8 (Casp8) suppresses receptor-interacting protein kinase-3 (RIPK3)/mixed lineage kinase domain-like (MLKL)-dependent necroptosis, demonstrated by the genetic evidence that deletion of Ripk3 or Mlkl prevented embryonic lethality Casp8-deficient mice. However, detailed mechanisms which Casp8 deficiency triggers necroptosis during development remain unclear. In this article, we show caused formation RIPK1-RIPK3 necrosome in yolk sac, leading to vascularization defects, MLKL and...