Tetrahydroxystilbene glucoside relieves the chronic inflammatory pain by inhibiting neuronal apoptosis, microglia activation, and GluN2B overexpression in anterior cingulate cortex

Fan, Yongfei; Guan, Shao-yu; Lu, Luo; Li, Yanjiao; Yang, Le; Zhou, Xiuping; Guo, Guo-dong; Zhao, Ming; Yang, Qi; Liu, Gang

doi:10.1177/1744806918814367

Cited by 22 publications

(16 citation statements)

References 48 publications

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“…Treatment with SP could relieve anxiety-like symptoms in CFA-injected mice and reduce the levels of pro-inflammatory cytokines, which is consistent with previous findings showing that SP exerts anti-inflammatory effects. Moreover, previous studies have demonstrated that CFA injection activates the microglia, the primary inflammatory mediators and main source of cytokines in the CNS [23]. The same was observed in the current study, and SP was found to reduce CFA-induced microglial activation in the BLA.…”

Section: Discussionsupporting

confidence: 91%

“…Moreover, scopoletin suppresses p-JNK and p-p38 MAPKs, which may act alone or relate to the activation of NF-κB [18]. Our previous studies have shown that the expression of NF-κB p65, p-p38, and p-JNK MAPKs is increased in mice with chronic inflammation induced by CFA [23,49]. These alterations were consistently confirmed in the present work, while SP treatment effectively reversed these alterations.…”

Section: Discussionsupporting

confidence: 88%

“…The animals were sacrificed, and the tissue samples from the bilateral BLA amygdala were dissected from brain slices under an anatomical microscope immediately after the behavioral tests. Western blot analysis was performed as previously described [23]. BLA samples were homogenized in ice-cold RIPA lysis buffer containing phosphatase and protease inhibitors.…”

Section: Western Blot Analysismentioning

confidence: 99%

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Scopoletin ameliorates anxiety-like behaviors in complete Freund’s adjuvant-induced mouse model

Sun

Yang

et al. 2020

Mol Brain

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Anxiety disorder is highly prevalent worldwide and represents a chronic and functionally disabling condition, with high levels of psychological stress characterized by cognitive and physiological symptoms. Scopoletin (SP), a main active compound in Angelica dahurica, is traditionally used for the treatment of headache, rhinitis, pain, and other conditions. Here, we evaluated the effects of SP in a mouse model of complete Freund's adjuvant (CFA)-induced chronic inflammation anxiety. SP (2.0, 10.0, 50.0 mg/kg) administration for 2 weeks dose-dependently ameliorated CFA-induced anxiety-like behaviors in the open field test and elevated plus maze test. Moreover, we found that SP treatment inhibited microglia activation and decreased both peripheral and central IL-1β, IL-6, and TNF-α levels in a dose-dependent manner. Additionally, the imbalance in excitatory/inhibitory receptors and neurotransmitters in the basolateral nucleus after CFA injection was also modulated by SP administration. Our findings indicate that the inhibition of the nuclear factor-kappa B and mitogen-activated protein kinase signaling pathways involving antiinflammatory activities and regulation of the excitatory/inhibitory balance can be attributed to the anxiolytic effects of SP. Moreover, our molecular docking analyses show that SP also has good affinity for gamma-aminobutyric acid (GABA) transaminase and GABA A receptors. Therefore, these results suggest that SP could be a candidate compound for anxiolytic therapy and for use as a structural base for developing new drugs.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 88%

Section: Western Blot Analysismentioning

confidence: 99%

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Scopoletin ameliorates anxiety-like behaviors in complete Freund’s adjuvant-induced mouse model

Sun

Yang

et al. 2020

Mol Brain

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“…Several pharmacological tools targeting glutamatergic signaling induce antinociceptive and/or anxiolytic effects in inflammation, presumably by inhibiting the upregulation of GluR1, NR2A, and NR2B in the ACC, as well as by reducing microglia and astrocyte activation and the induction of proinflammatory cytokines [261][262][263]. However, since these potential drugs are so far not directly applied to the ACC, accounting for other effects is challenging and more specific approaches are necessary to target specific neuron populations and their locations within defined brain regions to provide more mechanistic understanding.…”

Section: Glutamatementioning

confidence: 99%

The Medial Prefrontal Cortex as a Central Hub for Mental Comorbidities Associated with Chronic Pain

Kummer

Mitrić

Kalpachidou

et al. 2020

IJMS

100

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Chronic pain patients frequently develop and suffer from mental comorbidities such as depressive mood, impaired cognition, and other significant constraints of daily life, which can only insufficiently be overcome by medication. The emotional and cognitive components of pain are processed by the medial prefrontal cortex, which comprises the anterior cingulate cortex, the prelimbic, and the infralimbic cortex. All three subregions are significantly affected by chronic pain: magnetic resonance imaging has revealed gray matter loss in all these areas in chronic pain conditions. While the anterior cingulate cortex appears hyperactive, prelimbic, and infralimbic regions show reduced activity. The medial prefrontal cortex receives ascending, nociceptive input, but also exerts important top-down control of pain sensation: its projections are the main cortical input of the periaqueductal gray, which is part of the descending inhibitory pain control system at the spinal level. A multitude of neurotransmitter systems contributes to the fine-tuning of the local circuitry, of which cholinergic and GABAergic signaling are particularly emerging as relevant components of affective pain processing within the prefrontal cortex. Accordingly, factors such as distraction, positive mood, and anticipation of pain relief such as placebo can ameliorate pain by affecting mPFC function, making this cortical area a promising target region for medical as well as psychosocial interventions for pain therapy.

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“…Management of chronic pain remains a major medical challenge (Duan et al., 2018). Chronic pain has a negative impact on patient's life by altering general functions and activity, often affecting the prognosis of patients (Fan et al., 2018; Li et al., 2019; Xu et al., 2019). Inflammatory pain is a result of peripheral tissue damage and persistent inflammation and characterized by allodynia and hyperalgesia both at the site of damage and in adjacent tissue.…”

Section: Introductionmentioning

confidence: 99%

MiRNA‐107 contributes to inflammatory pain by down‐regulating GLT‐1 expression in rat spinal dorsal horn

Zhang

et al. 2021

European Journal of Pain

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Background Inflammatory pain is a severe clinical problem that affects the quality of life in patients. However, the currently available treatments for inflammatory pain have limited effect and even causes severe side effects. The aim of this study was to investigate the roles of miRNA‐107 and glutamate transporter 1 (GLT‐1) in the inflammatory pain of rats induced by complete Freund's adjuvant (CFA). Methods Paw withdrawal threshold (PWT) of rats was measured by von Frey Filaments. The expressions of miRNA‐107 and GLT‐1 in the lumbar spinal dorsal horn (L4‐L6) were measured with real‐time quantitative PCR and western blotting analysis. Fluorescent in situ hybridization and fluorescent‐immunohistochemistry were employed to detect the expression of miRNA‐107, GLT‐1 and co‐location of miRNA‐107 with GLT‐1. Results Injection of CFA significantly reduced PWT of rats. The miRNA‐107 expression level was obviously up‐regulated while the GLT‐1 expression level was decreased in the spinal dorsal horn of CFA rats. miRNA‐107 and GLT‐1 were co‐expressed in the same cells of the spinal dorsal horn in CFA rats. Ceftriaxone, a selective activator of GLT‐1, obviously increased the PWT of CFA rats. Furthermore, antagomir of miRNA‐107 reversed the down‐regulation of GLT‐1 and alleviated CFA‐induced mechanical allodynia of CFA rats. Conclusions These results suggest that an increase of miR‐107 contributes to inflammatory pain through downregulating GLT‐1 expression, implying a promising strategy for pain therapy. Significance The currently available treatments for inflammatory pain has limited effect even causes severe side effects. MiRNAs may have important diagnostic and therapeutic potential in inflammatory pain. In present study, we show a potential spinal mechanism of allodynia in rat inflammatory pain model induced by CFA. Increased miR‐107 contribute to inflammatory pain by targeting and downregulating GLT‐1 expression, implying a promising strategy for inflammatory pain.

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Tetrahydroxystilbene glucoside relieves the chronic inflammatory pain by inhibiting neuronal apoptosis, microglia activation, and GluN2B overexpression in anterior cingulate cortex

Cited by 22 publications

References 48 publications

Scopoletin ameliorates anxiety-like behaviors in complete Freund’s adjuvant-induced mouse model

Scopoletin ameliorates anxiety-like behaviors in complete Freund’s adjuvant-induced mouse model

The Medial Prefrontal Cortex as a Central Hub for Mental Comorbidities Associated with Chronic Pain

MiRNA‐107 contributes to inflammatory pain by down‐regulating GLT‐1 expression in rat spinal dorsal horn

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