Effects of chlorogenic acid on voltage-gated potassium channels of trigeminal ganglion neurons in an inflammatory environment

Liu, Fei; Lu, Xionggang; Zhang, Yujiao; Kou, Liang; Song, Ning; Wu, Min-Ke; Wang, Min; Wang, Hang; Shen, Jiefei

doi:10.1016/j.brainresbull.2016.09.005

Cited by 19 publications

(9 citation statements)

References 43 publications

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“…49 We modified the protocol of TG isolation from SD rats (5–7 days) described in previous reports. 50 Extracted TGs were washed using ice-cold Hanks’ balanced salt solution (pH = 7.4; Sigma, USA) and minced into small pieces under a dissecting microscope in modified α-MEM medium containing collagenase I (1 mg·mL –1 , Solarbio, China) and trypsin (0.125%; Gibco, USA). At the end of the incubation, modified α-MEM medium containing foetal bovine serum (FBS, 10%; Gibco, Australia origin, USA) and antibiotics (100 μg·mL –1 penicillin and 100 μg·mL –1 streptomycin; Sigma, USA) was added to stop the digestion.…”

Section: Methodsmentioning

confidence: 99%

Activation of mitogen-activated protein kinases in satellite glial cells of the trigeminal ganglion contributes to substance P-mediated inflammatory pain

et al. 2019

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Inflammatory orofacial pain, in which substance P (SP) plays an important role, is closely related to the cross-talk between trigeminal ganglion (TG) neurons and satellite glial cells (SGCs). SGC activation is emerging as the key mechanism underlying inflammatory pain through different signalling mechanisms, including glial fibrillary acidic protein (GFAP) activation, phosphorylation of mitogen-activated protein kinase (MAPK) signalling pathways, and cytokine upregulation. However, in the TG, the mechanism underlying SP-mediated orofacial pain generated by SGCs is largely unknown. In this study, we investigated whether SP is involved in inflammatory orofacial pain by upregulating interleukin (IL)-1β and tumour necrosis factor (TNF)-α from SGCs, and we explored whether MAPK signalling pathways mediate the pain process. In the present study, complete Freund’s adjuvant (CFA) was injected into the whisker pad of rats to induce an inflammatory model in vivo. SP was administered to SGC cultures in vitro to confirm the effect of SP. Facial expression analysis showed that pre-injection of L703,606 (an NK-1 receptor antagonist), U0126 (an inhibitor of MAPK/extracellular signal-regulated kinase [ERK] kinase [MEK] 1/2), and SB203580 (an inhibitor of P38) into the TG to induce targeted prevention of the activation of the NK-1 receptor and the phosphorylation of MAPKs significantly suppressed CFA-induced inflammatory allodynia. In addition, SP promoted SGC activation, which was proven by increased GFAP, p-MAPKs, IL-1β and TNF-α in SGCs under inflammatory conditions. Moreover, the increase in IL-1β and TNF-α was suppressed by L703, 606, U0126 and SB203580 in vivo and in vitro. These present findings suggested that SP, released from TG neurons, activated SGCs through the ERK1/2 and P38 pathways and promoted the production of IL-1β and TNF-α from SGCs, contributing to inflammatory orofacial pain associated with peripheral sensitization.

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Section: Methodsmentioning

confidence: 99%

Activation of mitogen-activated protein kinases in satellite glial cells of the trigeminal ganglion contributes to substance P-mediated inflammatory pain

et al. 2019

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“…This, in turn, is regulated by the function of various membrane ion channels, including sodium channels (Berta et al., 2008), calcium channels (Lu, Zhang, Luo, & Gold, 2010), and as mentioned above, potassium channels (Cao, Chen, Li, & Pan, 2012; Chien, Cheng, Chu, Cheng, & Tsaur, 2007; Mucha et al., 2010; Passmore et al., 2003). Potassium channels have been extensively studied for their effect in neuronal excitability and pain hypersensitivity, and have attracted increasing attention in recent years (Chien et al., 2007; Du, Gao, Jaffe, Zhang, & Gamper, 2018; Liu et al., 2016; Passmore et al., 2003). Several studies have verified a prolonged decline in Kv1.2 expression during nerve injury‐induced pain, which is consistent with our results (Everill & Kocsis, 2000; Fan et al., 2014; Kim, Choi, Rim, & Cho, 2002; Laumet et al., 2015; Liang et al., 2016; Zhao et al., 2013, 2017).…”

Section: Discussionmentioning

confidence: 99%

“…Kv1.2, as the first eukaryotic voltage‐gated channel with a reported atomic resolution structure, has been verified to play a crucial role in maintaining neuronal excitability through holding the resting membrane potential and mediating repolarization after action potentials (Baronas, Yang, Morales, Sipione, & Kurata, 2018; Gao & Ziskind‐Conhaim, 1998; Long, Campbell, & Mackinnon, 2005). It is reported that Kv1.2 expression in DRG is decreased in inflammation‐ or nerve injury‐induced pain and may contribute to the development of neuropathic pain (Fan et al., 2014; Liang et al., 2016; Liu et al., 2016; Lutz, Bekker, & Tao, 2014). However, the way in which Kv1.2 is down‐regulated in neuropathic pain still remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Epigenetic restoration of voltage‐gated potassium channel Kv1.2 alleviates nerve injury‐induced neuropathic pain

Zhang

Rong

Shao

et al. 2020

Journal of Neurochemistry

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Voltage‐gated potassium channels (Kv) are important regulators of neuronal excitability for its role of regulating resting membrane potential and repolarization. Recent studies show that Kv channels participate in neuropathic pain, but the detailed underlying mechanisms are far from being clear. In this study, we used siRNA, miR‐137 agomir, and antagomir to regulate the expression of Kv1.2 in spinal cord and dorsal root ganglia (DRG) of naïve and chronic constriction injury (CCI) rats. Kv currents and neuron excitability in DRG neurons were examined by patch‐clamp whole‐cell recording to verify the change in Kv1.2 function. The results showed that Kv1.2 was down‐regulated in DRG and spinal dorsal horn (SDH) by CCI. Knockdown of Kv1.2 by intrathecally injecting Kcna2 siRNA induced significant mechanical and thermal hypersensitivity in naïve rats. Concomitant with the down‐regulation of Kv1.2 was an increase in the expression of the miR‐137. The targeting and regulating of miR‐137 on Kcna2 was verified by dual‐luciferase reporter system and intrathecal injecting miR‐137 agomir. Furthermore, rescuing the expression of Kv1.2 in CCI rats, achieved through inhibiting miR‐137, restored the abnormal Kv currents and excitability in DRG neurons, and alleviated mechanical allodynia and thermal hyperalgesia. These results indicate that the miR‐137‐mediated Kv1.2 impairment is a crucial etiopathogenesis for the nerve injury‐induced neuropathic pain and can be a novel potential therapeutic target for neuropathic pain management.

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“…One particular constituent of coffee, chlorogenic acid, has been shown to modulate trigeminal neuron signaling in both in vitro 44 and in vivo 45 pain models. In a human trial comparing decaffeinated green coffee and isolated chlorogenic acid, headache (unspecified type) was significantly reduced by both substances compared to placebo after 2 hours.…”

Section: Poignant Quotesmentioning

confidence: 99%

“You will eat shoe polish if you think it would help”—Familiar and lesser‐known themes identified from mixed‐methods analysis of a cluster headache survey

et al. 2021

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Objective: To characterize patient-reported ideas and concerns about cluster headache, treatment options, and management strategies. Background: Cluster headache patients experience severe pain and often suffer additional consequences from their disease. Patients have identified methods to cope with and combat cluster headache that are not widely known. Methods: Secondary analysis was performed using deidentified data from the online Clusterbusters Medication Use survey, wherein 10 questions allowed for freely written comments. Using mixed-methods techniques, neurologists with expertise in headache medicine identified themes from these comments. Subgroup analysis sought to identify variables associated with specific themes. Results: Among 2274 free-text responses from 493 adult participants, 23 themes were identified. Themes commonly discussed in the literature included such topics as "nothing worked" (24.7%, 122/493), "side effects" (12.8%, 63/493), and difficulties with "access/cost" (2.4%, 12/493). Less widely recognized themes included the use of "illicit substances" (35.5%, 175/493) and "vitamins/supplements" (12.2%, 60/493) in disease management. Lesser-known themes included "coffee" (5.3%, 26/493) and "exercise/physical activity" (4.7%, 23/493). Using strict significance criteria, no subgroup was associated with any theme. Several poignant quotes highlighted patient thoughts and experiences. Conclusions: This mixed-methods analysis identified challenges endured by cluster headache patients, as well as a variety of patient-directed disease management approaches. The volunteered information spotlights pharmacological, physiological, and psychological aspects of cluster headache that warrant further exploratory and interventional investigation.

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Effects of chlorogenic acid on voltage-gated potassium channels of trigeminal ganglion neurons in an inflammatory environment

Cited by 19 publications

References 43 publications

Activation of mitogen-activated protein kinases in satellite glial cells of the trigeminal ganglion contributes to substance P-mediated inflammatory pain

Activation of mitogen-activated protein kinases in satellite glial cells of the trigeminal ganglion contributes to substance P-mediated inflammatory pain

Epigenetic restoration of voltage‐gated potassium channel Kv1.2 alleviates nerve injury‐induced neuropathic pain

“You will eat shoe polish if you think it would help”—Familiar and lesser‐known themes identified from mixed‐methods analysis of a cluster headache survey

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