Chronic constriction injury-induced nociception is relieved by nanomedicine-mediated decrease of rat hippocampal tumor necrosis factor

Gerard, Elizabeth E.; Spengler, Robert N.; Bonoiu, Adela C.; Mahajan, Supriya D.; Davidson, Bruce A.; Ding, Hong; Kumar, Rajiv; Prasad, Paras N.; Knight, Paul R.; Ignatowski, Tracey A.

doi:10.1097/j.pain.0000000000000181

Cited by 47 publications

(34 citation statements)

References 88 publications

(136 reference statements)

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“…In addition to the spinal cord, the DRG participate in the regulation of neuroimmune responses in neuropathic pain, as demonstrated by the differential expression of inflammatory neuropeptides and altered activation of peripheral immune cells in this region after painful injury [24, 25]. The hippocampus, a key integration site for pain signals, regulates CCI-induced pain behavior in rats [26]. Based on this evidence, we focused on investigating astrocyte activation and related inflammatory mechanisms in the DRG, spinal cord, and hippocampus of CCI-treated rats.…”

Section: Discussionmentioning

confidence: 99%

Hyperbaric oxygen attenuates neuropathic pain and reverses inflammatory signaling likely via the Kindlin-1/Wnt-10a signaling pathway in the chronic pain injury model in rats

Zhao

Pan

2017

J Headache Pain

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BackgroundHyperbaric oxygen (HBO) therapy is proven to attenuate neuropathic pain in rodents. The goal of the present study was to determine the potential involvement of the Kindlin-1/Wnt-10a signaling pathway during astrocyte activation and inflammation in a rodent model of neuropathic pain.MethodsRats were assigned into sham operation, chronic constriction injury (CCI), and CCI + HBO treatment groups. Neuropathic pain developed in rats following CCI of the sciatic nerve. Rats in the CCI + HBO group received HBO treatment for five consecutive days beginning on postoperative day 1. The mechanical withdrawal threshold (MWT) and the thermal withdrawal latency (TWL) tests were performed to determine mechanical and heat hypersensitivity of animals, respectively. Kindlin-1, Wnt-10a and β-catenin protein expression was examined by immunohistochemistry and Western blot analysis. Expression of tumor necrosis factor (TNF)-α was also determined by ELISA.ResultsOur findings demonstrated that HBO treatment significantly suppressed mechanical and thermal hypersensitivity in the CCI neuropathic pain model in rats. HBO therapy significantly reversed the up-regulation of Kindlin-1 in dorsal root ganglia (DRG), spinal cord, and hippocampus of CCI rats. CCI-induced astrocyte activation and increased levels of TNF-α were efficiently reversed by HBO (P < 0.05 vs. CCI). HBO also reversed Wnt-10a up-regulation induced by CCI in the DRG, spinal cord, and hippocampus (P < 0.05 vs. CCI).ConclusionsOur findings demonstrate that HBO attenuated CCI-induced rat neuropathic pain and inflammatory responses, possibly through regulation of the Kindlin-1/Wnt-10a signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Hyperbaric oxygen attenuates neuropathic pain and reverses inflammatory signaling likely via the Kindlin-1/Wnt-10a signaling pathway in the chronic pain injury model in rats

Zhao

Pan

2017

J Headache Pain

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“…It was reported that tumor necrosis factor-α (TNF-α), which binds to tumor necrosis factor receptor 1 (TNFR1) and induces NF-kB and p38 MAPK activation, was also upregulated following peripheral nerve injury [ 82 , 83 ]. Therefore, Lee et al [ 84 ] investigated whether TNFR1 regulates IL-6 expression through NF-kB or p38 MAPK activation in the spinal cord and DRG using a CCI model.…”

Section: Il-6 and Peripheral Nerve Injurymentioning

confidence: 99%

Interleukin-6: an emerging regulator of pathological pain

Zhou

Liu

et al. 2016

J Neuroinflammation

317

226

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Interleukin-6 is an inflammatory cytokine with wide-ranging biological effects. It has been widely demonstrated that neuroinflammation plays a critical role in the development of pathological pain. Recently, various pathological pain models have shown elevated expression levels of interleukin-6 and its receptor in the spinal cord and dorsal root ganglia. Additionally, the administration of interleukin-6 could cause mechanical allodynia and thermal hyperalgesia, and an intrathecal injection of anti-interleukin-6 neutralizing antibody alleviated these pain-related behaviors. These studies indicated a pivotal role of interleukin-6 in pathological pain. In this review, we summarize the recent progress in understanding the roles and mechanisms of interleukin-6 in mediating pathological pain associated with bone cancer, peripheral nerve injury, spinal cord injury, chemotherapy-induced peripheral neuropathy, complete Freund’s adjuvant injection, and carrageenan injection. Understanding and regulating interleukin-6 could be an interesting lead to novel therapeutic strategies for pathological pain.

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“…The following list provides an overview of examples of specific anti-TNF biologicals in various stages of development or in use for treating disease: Systemic disease: rheumatoid arthritis [ 63 , 64 ], psoriasis [ 66 , 114 , 115 ], Crohn's disease [ 116 ], spondyloarthritis [ 117 ], Jarisch-Herxheimer's disease [ 35 , 51 ], graft-versus-host disease [ 56 , 118 ], reaction to OKT-3 [ 53 , 54 ]. Chronic CNS disease: pain [ 77 – 79 , 81 , 113 , 119 – 123 ], Alzheimer's disease [ 89 , 124 ], Parkinson's disease [ 125 ], Huntington disease [ 126 ], post-LPS cognition [ 127 ], postoperative cognition [ 108 ], postirradiation cognition [ 109 ], postchemotherapy cognition [ 110 ], rheumatoid arthritis cognition [ 112 ], sarcoidosis cognition [ 111 ], poststroke therapy [ 69 , 87 , 97 , 98 ], traumatic brain injury [ 69 , 83 ]. …”

Section: The Narrow Vision Of the Traditional Anatomical Focus Of mentioning

confidence: 99%

“… pain [ 77 – 79 , 81 , 113 , 119 – 123 ], Alzheimer's disease [ 89 , 124 ], Parkinson's disease [ 125 ], Huntington disease [ 126 ], post-LPS cognition [ 127 ], postoperative cognition [ 108 ], postirradiation cognition [ 109 ], postchemotherapy cognition [ 110 ], rheumatoid arthritis cognition [ 112 ], sarcoidosis cognition [ 111 ], poststroke therapy [ 69 , 87 , 97 , 98 ], traumatic brain injury [ 69 , 83 ]. …”

Section: The Narrow Vision Of the Traditional Anatomical Focus Of mentioning

confidence: 99%

A Neurologist’s Guide to TNF Biology and to the Principles behind the Therapeutic Removal of Excess TNF in Disease

Clark

Vissel

2015

Neural Plasticity

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Tumor necrosis factor (TNF) is an ancient and widespread cytokine required in small amounts for much physiological function. Higher concentrations are central to innate immunity, but if unchecked this cytokine orchestrates much chronic and acute disease, both infectious and noninfectious. While being a major proinflammatory cytokine, it also controls homeostasis and plasticity in physiological circumstances. For the last decade or so these principles have been shown to apply to the central nervous system as well as the rest of the body. Nevertheless, whereas this approach has been a major success in treating noncerebral disease, its investigation and potential widespread adoption in chronic neurological conditions has inexplicably stalled since the first open trial almost a decade ago. While neuroscience is closely involved with this approach, clinical neurology appears to be reticent in engaging with what it offers patients. Unfortunately, the basic biology of TNF and its relevance to disease is largely outside the traditions of neurology. The purpose of this review is to facilitate lowering communication barriers between the traditional anatomically based medical specialties through recognition of shared disease mechanisms and thus advance the prospects of a large group of patients with neurodegenerative conditions for whom at present little can be done.

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Chronic constriction injury-induced nociception is relieved by nanomedicine-mediated decrease of rat hippocampal tumor necrosis factor

Cited by 47 publications

References 88 publications

Hyperbaric oxygen attenuates neuropathic pain and reverses inflammatory signaling likely via the Kindlin-1/Wnt-10a signaling pathway in the chronic pain injury model in rats

Hyperbaric oxygen attenuates neuropathic pain and reverses inflammatory signaling likely via the Kindlin-1/Wnt-10a signaling pathway in the chronic pain injury model in rats

Interleukin-6: an emerging regulator of pathological pain

A Neurologist’s Guide to TNF Biology and to the Principles behind the Therapeutic Removal of Excess TNF in Disease

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