COX-2 contributed to the remifentanil-induced hyperalgesia related to ephrinB/EphB signaling

Peng, Yunan; Zang, Ting; Zhou, Lei; Ni, Kun; Zhou, Xi‐Lang

doi:10.1080/01616412.2019.1580459

Cited by 9 publications

(4 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Li et al also found that microRNA-212-3p controls peripheral neuropathic allodynia and sodium voltage-gated channel alpha subunit 3 (Nav 1.3) through inhibiting caspase-3 cleavage and B-cell lymphoma 2-associated X apoptosis regulator (BAX) expression in rats with CCI surgery ( Li Y. et al, 2019 ). EphrinB/EphB signaling, the most important subfamily of receptor tyrosine kinases (RTKs) in humans, is one of pivotal cascades in the spinal pain processing and nociceptive synaptic plasticity ( Deng et al, 2017 ; Peng et al, 2019 ). Recent evidence discloses that caspase-3 activation in the spinal dorsal horn neurons but not microglia and astrocyte is implicated in EphrinB/EphB signaling dependent neuropathic pain formation in a mouse model of CCI ( Yang et al, 2018 ) ( Table 2 ).…”

Section: Caspases and Neuropathic Painmentioning

confidence: 99%

The Involvement of Caspases in Neuroinflammation and Neuronal Apoptosis in Chronic Pain and Potential Therapeutic Targets

Zhang

et al. 2022

Front. Pharmacol.

View full text Add to dashboard Cite

Chronic pain is a common, complex and unpleasant sensation following nerve injury, tissue trauma, inflammatory diseases, infection and cancer. It affects up to 25% of adults and is increasingly recognized as the leading cause of distress, disability and disease burden globally. Chronic pain is often refractory to most current analgesics, thus emphasizing the requirement for improved therapeutic medications. It is of great importance to elucidate the specific pathogenesis of chronic pain with different etiologies. Recent progress has advanced our understanding in the contribution of neuroinflammation and glial cells (microglia and astrocyte) activation in the plasticity of excitatory nociceptive synapses and the development of chronic pain phenotypes. Oxidative stress-associated neuronal apoptosis is also identified to be a pivotal step for central pain sensitization. The family of cysteine aspartate specific proteases (Caspases) has been well known to be key signaling molecules for inflammation and apoptosis in several neurological conditions. Recent studies have highlighted the unconventional and emerging role of caspases in microgliosis, astrocytes morphogenesis, chemokines release, cytokines secretion and neuronal apoptosis in initiating and maintaining synaptogenesis, synaptic strength and signal transduction in persistent pain hypersensitivity, suggesting the possibility of targeting caspases pathway for prevention and treatment of chronic pain. In this review, we will discuss and summarize the advances in the distinctive properties of caspases family in the pathophysiology of chronic pain, especially in neuropathic pain, inflammatory pain, cancer pain and musculoskeletal pain, with the aim to find the promising therapeutic candidates for the resolution of chronic pain to better manage patients undergoing chronic pain in clinics.

show abstract

Section: Caspases and Neuropathic Painmentioning

confidence: 99%

The Involvement of Caspases in Neuroinflammation and Neuronal Apoptosis in Chronic Pain and Potential Therapeutic Targets

Zhang

et al. 2022

Front. Pharmacol.

View full text Add to dashboard Cite

show abstract

“…As such, NSAIDs have been demonstrated to inhibit the heightened sensitivity to pain triggered by the activation of spinal NMDA and substance P receptors ( Malmberg and Yaksh, 1992 ; Yaksh and Malmberg, 1993 ). Clinical studies or meta-analyses about the effect of COX inhibitors on OIH are still lacking, even though it has been proved in animal models ( Li et al, 2018 ; Peng et al, 2019 ) and human volunteers ( Koppert et al, 2004 ; Lenz et al, 2011 ).…”

Section: Discussionmentioning

confidence: 99%

Pharmacological interventions for preventing opioid-induced hyperalgesia in adults after opioid-based anesthesia: a systematic review and network meta-analysis

et al. 2023

View full text Add to dashboard Cite

Background: Opioid-induced hyperalgesia (OIH) is an adverse event of prolonged opioid use that increases pain intensity. The optimal drug to prevent these adverse effects is still unknown. We aimed to conduct a network meta-analysis to compare different pharmacological interventions for preventing the increase in postoperative pain intensity caused by OIH.Methods: Several databases were searched independently for randomized controlled trials (RCTs) comparing various pharmacological interventions to prevent OIH. The primary outcomes were postoperative pain intensity at rest after 24 h and the incidence of postoperative nausea and vomiting (PONV). Secondary outcomes included pain threshold at 24 h after surgery, total morphine consumption over 24 h, time to first postoperative analgesic requirement, and shivering incidence.Results: In total, 33 RCTs with 1711 patients were identified. In terms of postoperative pain intensity, amantadine, magnesium sulphate, pregabalin, dexmedetomidine, ibuprofen, flurbiprofen plus dexmedetomidine, parecoxib, parecoxib plus dexmedetomidine, and S (+)-ketamine plus methadone were all associated with milder pain intensity than placebo, with amantadine being the most effective (SUCRA values = 96.2). Regarding PONV incidence, intervention with dexmedetomidine or flurbiprofen plus dexmedetomidine resulted in a lower incidence than placebo, with dexmedetomidine showing the best result (SUCRA values = 90.3).Conclusion: Amantadine was identified as the best in controlling postoperative pain intensity and non-inferior to placebo in the incidence of PONV. Dexmedetomidine was the only intervention that outperformed placebo in all indicators.Clinical Trial Registration:https://www.crd.york.ac. uk/prospero/display_record.php?, CRD42021225361.

show abstract

“…Former studies have investigated the mechanism of Remi-stimulated hyperalgesia. For instance, Yunan Peng et al have pointed out that COX-2 contributes to Remi-stimulated hyperalgesia related to ephrinB/EphB signaling (23). Linlin Zhang et al have found that intrathecal injection of artesunate impairs Remi-stimulated hyperalgesia by down-regulating spinal mGluR5 expression in rats (24).…”

Section: Discussionmentioning

confidence: 99%

SIRT2 overexpression decreases remifentanil-stimulated post-surgical hyperalgesia via microglia

Wei Zhu,

Zhengliang Ma

2023

Cell Mol Biol (Noisy-le-grand)

View full text Add to dashboard Cite

COX-2 contributed to the remifentanil-induced hyperalgesia related to ephrinB/EphB signaling

Cited by 9 publications

References 50 publications

The Involvement of Caspases in Neuroinflammation and Neuronal Apoptosis in Chronic Pain and Potential Therapeutic Targets

The Involvement of Caspases in Neuroinflammation and Neuronal Apoptosis in Chronic Pain and Potential Therapeutic Targets

Pharmacological interventions for preventing opioid-induced hyperalgesia in adults after opioid-based anesthesia: a systematic review and network meta-analysis

SIRT2 overexpression decreases remifentanil-stimulated post-surgical hyperalgesia via microglia

Contact Info

Product

Resources

About