Cynandione A Alleviates Neuropathic Pain Through α7-nAChR-Dependent IL-10/β-Endorphin Signaling Complexes

Han, Qiaoqiao; Yin, Min; Wang, Ziying; Líu, Hao; Ao, Junping; Wang, Yongxiang

doi:10.3389/fphar.2020.614450

Cited by 9 publications

(8 citation statements)

References 64 publications

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“…Accordingly, it has been demonstrated that increased IL-10 gene expression after exenatide administration is mediated by the cAMP/PKA/p38/CREB pathway [31]. Similar results were observed in mice, where the underlying mechanism of IL-10 release via α7-nAChR activation by cynandione also occurred through the cAMP/PKA/p38/CREB pathway [37]. IL-10 acts autocrinely when released by microglia, activating STAT3, which induces β-endorphin gene expression [31,36,37].…”

Section: Spinal Microglial Activation Increases Il-10/β-endorphin Levelsmentioning

confidence: 65%

“…Recent evidence has demonstrated IL-10 and β-endorphin impact on pain control [30,[34][35][36][37][38][39][40][41][42][43]. Thus, studies analyzing these two protagonists were selected, in which microglia proved to be the main cell involved in this process, as shown in Table 1, Figure 2, and the graphical abstract.…”

Section: Pain Control By Il-10 Via β-Endorphin Release At the Spinal ...mentioning

confidence: 99%

“…Increased IL-10 and β-endorphin spinal cord levels seem to attenuate this hyperexcitability [35]. Furthermore, spinal activation of glucagon-like peptide-1 receptor (GLP-1R), G protein-coupled receptor 40 (GPR40), and alpha-7 nicotinic acetylcholine receptor (α7-nAChR) has been shown to elevate IL-10 and β-endorphin levels, resulting in an antinociceptive effect [31,[36][37][38][39][40].…”

Section: Spinal Microglial Activation Increases Il-10/β-endorphin Levelsmentioning

confidence: 99%

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IL-10/β-Endorphin-Mediated Neuroimmune Modulation on Microglia during Antinociception

et al. 2023

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Microglia are glial cells centrally related to pathophysiology and neuroimmunological regulation of pain through microglia–neuron crosstalk mechanisms. In contrast, anti-inflammatory mechanisms guided by immunological effectors such as IL-10 trigger the secretion of analgesic substances, culminating in the differential expression of genes encoding endogenous opioid peptides, especially β-endorphin. Thus, when β-endorphin binds to the µ-opioid receptor, it generates neuronal hyperpolarization, inhibiting nociceptive stimuli. This review aimed to summarize the recent advances in understanding the mechanism by which IL-10/β-endorphin can reduce pain. For this, databases were searched for articles from their inception up until November 2022. Two independent reviewers extracted the data and assessed the methodological quality of the included studies, and seventeen studies were considered eligible for this review. Several studies have demonstrated the impact of IL-10/β-endorphin in reducing pain, where IL-10 can stimulate GLP-1R, GRP40, and α7nAChR receptors, as well as intracellular signaling pathways, such as STAT3, resulting in increased β-endorphin expression and secretion. In addition, molecules such as gabapentinoids, thalidomide, cynandione A, morroniside, lemairamin, and cinobufagin, as well as non-pharmacological treatments such as electroacupuncture, reduce pain through IL-10 mediated mechanisms, reflecting a microglia-dependent β-endorphin differential increase. This process represents a cornerstone in pain neuroimmunology knowledge, and the results obtained by different studies about the theme are presented in this review.

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Section: Spinal Microglial Activation Increases Il-10/β-endorphin Levelsmentioning

confidence: 65%

Section: Pain Control By Il-10 Via β-Endorphin Release At the Spinal ...mentioning

confidence: 99%

Section: Spinal Microglial Activation Increases Il-10/β-endorphin Levelsmentioning

confidence: 99%

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IL-10/β-Endorphin-Mediated Neuroimmune Modulation on Microglia during Antinociception

et al. 2023

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“…Moreover, α7 nAChR agonists and allosteric modulators suppressed the release of proinflammatory cytokines in chronic pain models (Loram et al, 2010;Sun et al, 2017). More importantly, α7 nAChR agonists and allosteric modulators have shown potent analgesic effects (Bagdas et al, 2018b;Quadri et al, 2018;Wang et al, 2019;Arias et al, 2020;Han et al, 2020). Therefore, it is plausible that potentiation of the α7 nAChR may be a promising therapeutic strategy for the management of chronic pain.…”

Section: Introductionmentioning

confidence: 99%

Targeting α7 nicotinic acetylcholine receptors for chronic pain

Zhou

Liu²,

Liu³

et al. 2022

Front. Mol. Neurosci.

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Despite rapid advances in the field of chronic pain, it remains extremely challenging in the clinic. Pain treatment strategies have not improved for decades as opioids remain the main prescribed drugs for chronic pain management. However, long-term use of opioids often leads to detrimental side effects. Therefore, uncovering the mechanisms underlying the development and maintenance of chronic pain may aid the discovery of novel therapeutics to benefit patients with chronic pain. Substantial evidence indicates downregulation of α7 nicotinic acetylcholine receptors (α7 nAChR) in the sciatic nerve, dorsal root ganglia, and spinal cord dorsal horn in rodent models of chronic pain. Moreover, our recent study and results from other laboratories demonstrate that potentiation of α7 nAChR attenuates pain behaviors in various murine models of chronic pain. This review summarized and discussed the preclinical evidence demonstrating the therapeutic potential of α7 nAChR agonists and allosteric modulators in chronic pain. This evidence indicates that potentiation of α7 nAChR is beneficial in chronic pain, mostly by alleviating neuroinflammation. Overall, α7 nAChR-based therapy for chronic pain is an area with great promise, but more research regarding its detailed mechanisms is warranted.

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“…Cynandione A, a dimeric acetophenone that can be classified as abridged phenylpropanoid, or plant phenolics, is usually metabolized from tyrosine. It is an important bioactive marker of Cynanchum species, and was shown to possess neuroprotective [10,11], anti-inflammatory [11,12], hepatoprotective [13], and hypoglycemic [14] activities, as well as attenuating neuropathic pain [15].…”

Section: Introductionmentioning

confidence: 99%

Responses of Cynanchum taiwanianum and Its Bioactive Compound Biosynthesis to Levels of Nitrogen and Potassium Fertilization

Tseng

2022

Agronomy

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Cynanchum taiwanianum is an important plant used in traditional medicine. The increasing demand and lack of information regarding its cultivation have become concerns for sustainability. This study examined the effects of nitrogen and potassium fertilization rates on the growth and biosynthesis of main bioactive compounds, including cynandione A and polyphenolic compounds, in field-cultivated C. taiwanianum. Two field experiments were conducted using three levels of nitrogen (N100, N150 and N200) and three levels of potassium (K100, K150 and K200) treatments. The experimental variables were either N or K fertilizer. The results showed that, aside from N200, N and K fertilization significantly increased C. taiwanianum shoot and tuber biomass. High N fertilization resulted in low total phenolic and total flavonoid contents in shoots and tubers, but the effects of K fertilization were minimal. Cynandione A, an important bioactive compound, was only detected in tubers; its content were enhanced with the increasing K fertilization, but reduced with excess N fertilization (N200). Although N and K fertilizers are important for C. taiwanianum tuber production, the yield of cynandione A was associated with K but not N fertilization rates. These results provide some essential information for the optimal production of C. taiwanianum tubers and functional compounds. Further studies are required to examine the mechanism(s) of cynandione A biosynthesis and its compartmentation in plant tissues.

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Cynandione A Alleviates Neuropathic Pain Through α7-nAChR-Dependent IL-10/β-Endorphin Signaling Complexes

Cited by 9 publications

References 64 publications

IL-10/β-Endorphin-Mediated Neuroimmune Modulation on Microglia during Antinociception

IL-10/β-Endorphin-Mediated Neuroimmune Modulation on Microglia during Antinociception

Targeting α7 nicotinic acetylcholine receptors for chronic pain

Responses of Cynanchum taiwanianum and Its Bioactive Compound Biosynthesis to Levels of Nitrogen and Potassium Fertilization

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