A5054279514- Pain Mechanisms and Treatments
- Neuropeptides and Animal Physiology
- Ion Channels and Receptors
- Botulinum Toxin and Related Neurological Disorders
- Nerve injury and regeneration
- Fatty Acid Research and Health
- Neuroscience and Neuropharmacology Research
- Eicosanoids and Hypertension Pharmacology
- Ion channel regulation and function
- Reproductive Physiology in Livestock
- Neuroinflammation and Neurodegeneration Mechanisms
- Reproductive Biology and Fertility
- Pharmacological Effects of Natural Compounds
- Genetic and phenotypic traits in livestock
- Exercise and Physiological Responses
- Receptor Mechanisms and Signaling
- Immune Response and Inflammation
- Hormonal and reproductive studies
- Bioactive Compounds and Antitumor Agents
- Inflammatory mediators and NSAID effects
- Asthma and respiratory diseases
- Plant-based Medicinal Research
- Parkinson's Disease Mechanisms and Treatments
- Cancer Treatment and Pharmacology
- Dermatology and Skin Diseases
Zhejiang University
2018-2025
First Affiliated Hospital Zhejiang University
2021-2025
Zhejiang Lab
2021-2025
Brain (Germany)
2024
Second Affiliated Hospital of Zhejiang University
2021-2022
Duke University Hospital
2013-2018
Duke Medical Center
2013-2018
Harvard University
2008-2016
Brigham and Women's Hospital
2008-2016
Duke University
2012-2014
Self-resolving inflammatory exudates and lipid mediator metabolomics recently uncovered a new family of potent anti-inflammatory proresolving mediators biosynthesized by macrophages (MΦs), denoted maresins. Here we determined that maresin 1 (MaR1) produced human MΦs from endogenous docosahexaenoic acid (DHA) matched synthetic 7R,14S-dihydroxydocosa-4Z,8E,10E,12Z,16Z,19Z-hexaenoic acid. The MaR1 alcohol groups Z/E geometry conjugated double bonds were using isomers prepared total organic...
Our previous study showed that activation of c-jun-N-terminal kinase (JNK) in spinal astrocytes plays an important role neuropathic pain sensitization. We further investigated how JNK regulates pain. In cultured astrocytes, tumor necrosis factor alpha (TNF-alpha) transiently activated via TNF receptor-1. Cytokine array indicated the chemokine CCL2/MCP-1 (monocyte chemoattractant protein-1) was strongly induced by TNF-alpha/JNK pathway. MCP-1 upregulation TNF-alpha dose dependently inhibited...
The objective of the present study was to characterize expression mRNAs encoding FSH and LH receptors during follicular development at different stages first wave in cattle. Following estrus, groups heifers (3–5 per group) were ovariectomized on day initiation (as determined by ultrasonography; Day 0), or Days 2, 4, 6, 8, 10 after wave. receptor detected within follicles ≥ 4 mm some smaller situ hybridization quantified image analysis. mRNA expressed granulosa cells all growing follicles,...
Inflammatory pain such as arthritic is typically treated with opioids and cyclo-oxygenase-2 inhibitors well known side effects. Transient receptor potential subtype vanilloid 1 (TRPV1) TRP ankyryn (TRPA1) contribute importantly to the genesis of inflammatory via both peripheral mechanisms (peripheral sensitization) spinal cord (central sensitization). Although these channels have been intensively studied, little about their endogenous inhibitors. Recent studies demonstrated that lipid...
The mechanisms of pain induction by inflammation have been extensively studied. However, the resolution are not fully understood. Here, we report that GPR37, expressed macrophages (MΦs) but microglia, contributes to inflammatory pain. Neuroprotectin D1 (NPD1) and prosaptide TX14 increase intracellular Ca2+ (iCa2+) levels in GPR37-transfected HEK293 cells. NPD1 also bind GPR37 cause GPR37-dependent iCa2+ increases peritoneal MΦs. Activation triggers MΦ phagocytosis zymosan particles via...
Mechanisms of inflammatory pain are not fully understood. We investigated the role TRPV1 (transient receptor potential subtype V1) and TNF-α, two critical mediators for pain, in regulating spinal cord synaptic transmission. found mice lacking Trpv1 frequency but amplitude spontaneous EPSCs (sEPSCs) lamina II neurons slices is reduced. Further, C-fiber-induced long-term potentiation (LTP) vivo abolished knock-out mice. TNF-α also increases sEPSC outer (lamina IIo) neurons, this increase...
Tumor necrosis factor-alpha (TNF-α) is a key proinflammatory cytokine. It generally believed that TNF-α exerts its effects primarily via TNF receptor subtype-1 (TNFR1). We investigated the distinct roles of TNFR1 and TNFR2 in spinal cord synaptic transmission inflammatory pain. Compared to wild-type (WT) mice, TNFR1- TNFR2-knockout (KO) mice exhibited normal heat sensitivity unaltered excitatory cord, as revealed by spontaneous postsynaptic currents lamina II neurons slices. However,...
It is generally accepted that ovarian follicular cysts (cysts) are nonovulatory structures contribute to extended calving intervals. Follicle/cyst dynamics and the etiology of unclear. The present study was conducted characterize follicle/cyst define endocrine changes (etiology) associated with cyst development. Thirty-two dairy cows were studied: controls (n = 6), spontaneously occurring 14), in which induced by exogenous steroid treatment 12). Ovaries scanned daily ultrasonography record...
Increasing evidence indicates that the pathogenesis of neuropathic pain is mediated through spinal cord microglia activation. The intracellular protease caspase-6 (CASP6) known to regulate neuronal apoptosis and axonal degeneration; however, contribution CASP6 in modulating synaptic transmission unclear. Here, we found expressed specifically C-fiber terminals superficial dorsal horn. Animals exposed intraplantar formalin or bradykinin injection exhibited activation Casp6-null mice had normal...
Itch, also known as pruritus, is a common, intractable symptom of several skin diseases, such atopic dermatitis and xerosis. TLRs mediate innate immunity regulate neuropathic pain, but their roles in pruritus are elusive. Here, we report that scratching behaviors induced by histamine-dependent -independent pruritogens markedly reduced mice lacking the Tlr3 gene. TLR3 expressed mainly small-sized primary sensory neurons dorsal root ganglions (DRGs) coexpress itch signaling pathway components...
To provide a tool to investigate the mechanisms inducing and maintaining cancer-related pain hyperalgesia, soft tissue tumor/metastasis model was developed that is applicable in C57BL/6J wild-type transgenic mice. We show experimental tumor-induced heat hyperalgesia nociceptor sensitization were prevented by systemic treatment with tumor necrosis factor α (TNFα) antagonist etanercept. In naive mice, exogenous TNFα evoked vivo sensitized nociceptive nerve fibers vitro . enhanced expression of...
Peripheral inflammation induces persistent central sensitization characterized by mechanical allodynia and heat hyperalgesia that are mediated distinct mechanisms. Compared to well-demonstrated mechanisms of hyperalgesia, underlying the development contralateral pain incompletely known. In this study, we investigated role spinal JNK in allodynia, an inflammatory model. Intraplantar injection complete Freund's adjuvant (CFA) induced bilateral but unilateral hyperalgesia. CFA also a activation...
Epoxyeicosatrienoic acids (EETs) are cytochrome P450-epoxygenase-derived metabolites of arachidonic acid that act as endogenous signaling molecules in multiple biological systems. Here we have investigated the specific contribution 5,6-EET to transient receptor potential (TRP) channel activation nociceptor neurons and its consequence for nociceptive processing. We found that, during capsaicin-induced nociception, levels increased dorsal root ganglia (DRGs) spinal cord, is released from...
Prevalence of neuropathic pain is high after major surgery. However, effective treatment for preventing lacking. Here we report that perisurgical neuroprotectin D1/protectin D1 (NPD1/PD1), derived from docosahexaenoic acid, prevents nerve injury-induced mechanical allodynia and ongoing in mice. Intrathecal post-treatment NPD1/PD1 also effectively reduces established produces no apparent signs analgesic tolerance. Mechanistically, blocks long-term potentiation, glial reaction, inflammatory...
The proinflammatory cytokine interleukin-17 (IL-17) is implicated in pain regulation. However, the synaptic mechanisms by which IL-17 regulates transmission are unknown. Here, we report that glia-produced suppresses inhibitory spinal cord circuit and drives chemotherapy-induced neuropathic pain. We find not only enhances excitatory postsynaptic currents (EPSCs) but also (IPSCs) GABA-induced lamina IIo somatostatin-expressing neurons mouse slices. mainly expresses astrocytes, its receptor...