Ghrelin may attenuate proinflammatory cytokine-mediated neuropathic pain

Güneli, Ensari; Kazıkdaş, Kadir Çağdaş; Kolatan, Efsun

doi:10.1016/j.mehy.2006.12.042

Cited by 23 publications

(18 citation statements)

References 47 publications

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“…Various studies have demonstrated that ghrelin exerts beneficial effects to inflammatory diseases because of its anti-inflammatory activity. Theil et al 14 29,30 also suggested that the neuroprotective effect of ghrelin appeared to associate with a reduction in proinflammatory cytokines in spinal cords with sciatic nerve injury. Consistent with these studies, our present results showed that intrathecal ghrelin markedly decreased the levels of TNF-α, IL-1β, and IL-6 in the spinal dorsal horns of CCI rats, and that these expression levels could be antagonized by a ghrelin receptor antagonist.…”

Section: Discussionmentioning

confidence: 99%

Ghrelin Alleviates Neuropathic Pain Through GHSR-1a–Mediated Suppression of the p38 MAPK/NF-κB Pathway in a Rat Chronic Constriction Injury Model

Zhou

Zhu

et al. 2014

Regional Anesthesia and Pain Medicine

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Section: Discussionmentioning

confidence: 99%

Ghrelin Alleviates Neuropathic Pain Through GHSR-1a–Mediated Suppression of the p38 MAPK/NF-κB Pathway in a Rat Chronic Constriction Injury Model

Zhou

Zhu

et al. 2014

Regional Anesthesia and Pain Medicine

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“…Originally, ghrelin’s role in pain sensitivity was thought to be through a combination of central and peripheral GHSR-1a signalling [153,154]. Chronic peripheral ghrelin administration has been shown to attenuate neuropathic pain in rats [155].…”

Section: Growth Hormone Secretagogue Receptor (Ghsr-1a) Receptor—bmentioning

confidence: 99%

From Belly to Brain: Targeting the Ghrelin Receptor in Appetite and Food Intake Regulation

Howick

Griffin

Cryan

et al. 2017

IJMS

126

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Ghrelin is the only known peripherally-derived orexigenic hormone, increasing appetite and subsequent food intake. The ghrelinergic system has therefore received considerable attention as a therapeutic target to reduce appetite in obesity as well as to stimulate food intake in conditions of anorexia, malnutrition and cachexia. As the therapeutic potential of targeting this hormone becomes clearer, it is apparent that its pleiotropic actions span both the central nervous system and peripheral organs. Despite a wealth of research, a therapeutic compound specifically targeting the ghrelin system for appetite modulation remains elusive although some promising effects on metabolic function are emerging. This is due to many factors, ranging from the complexity of the ghrelin receptor (Growth Hormone Secretagogue Receptor, GHSR-1a) internalisation and heterodimerization, to biased ligand interactions and compensatory neuroendocrine outputs. Not least is the ubiquitous expression of the GHSR-1a, which makes it impossible to modulate centrally-mediated appetite regulation without encroaching on the various peripheral functions attributable to ghrelin. It is becoming clear that ghrelin’s central signalling is critical for its effects on appetite, body weight regulation and incentive salience of food. Improving the ability of ghrelin ligands to penetrate the blood brain barrier would enhance central delivery to GHSR-1a expressing brain regions, particularly within the mesolimbic reward circuitry.

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“…Recently, investigations have focused on the role of central nervous system (CNS) immune responses after nerve injuries that lead to behavioral hypersensitivity 3-5. A current theory for the etiology of neuropathic pain involves CNS immune activation with cytokine production inducing the expression of final common pain mediators such as TNF-α and IL-1β 6-8.…”

Section: Introductionmentioning

confidence: 99%

Intrathecal siRNA against Toll-like receptor 4 reduces nociception in a rat model of neuropathic pain

Wu¹,

Bian²,

Miao³

et al. 2010

Int. J. Med. Sci.

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Background: Neuropathic pain is characterized by hyperalgesia, allodynia and spontaneous pain. It often occurs as a result of injury to peripheral nerves, dorsal root ganglions (DRG), spinal cord, or brain. Recent studies have suggested that Toll-like receptor 4 (TLR4) might play a role in neuropathic pain. Methodology/Principal Findings: In this study, we investigated the role of TLR4 in a rat chronic constriction injury (CCI) model and explored the feasibility of treating neuropathic pain by inhibiting TLR4. Our results demonstrated that intrathecal siRNA-mediated suppression of TLR4 attenuated CCI-induced mechanical allodynia and thermal hyperalgesia through inhibiting the activation of NF-κB p65 and production of proinflammatory cytokines (e.g., TNF-α and IL-1β). Conclusions/Significance: These findings suggest that suppression of TLR4 mediated by intrathecally administered siRNA may be a new strategy for the treatment of neuropathic pain.

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Ghrelin may attenuate proinflammatory cytokine-mediated neuropathic pain

Cited by 23 publications

References 47 publications

Ghrelin Alleviates Neuropathic Pain Through GHSR-1a–Mediated Suppression of the p38 MAPK/NF-κB Pathway in a Rat Chronic Constriction Injury Model

Ghrelin Alleviates Neuropathic Pain Through GHSR-1a–Mediated Suppression of the p38 MAPK/NF-κB Pathway in a Rat Chronic Constriction Injury Model

From Belly to Brain: Targeting the Ghrelin Receptor in Appetite and Food Intake Regulation

Intrathecal siRNA against Toll-like receptor 4 reduces nociception in a rat model of neuropathic pain

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