The Experts below are selected from a list of 20277 Experts worldwide ranked by ideXlab platform

Yingxia Liang - One of the best experts on this subject based on the ideXlab platform.

  • the high affinity igg receptor fcγri modulates Peripheral Nerve Injury induced neuropathic pain in rats
    Molecular Brain, 2019
    Co-Authors: Yingxia Liang, Zhiyu Zhang, Zhaodong Juan, Rui Zhang, Can Zhang
    Abstract:

    The Fc gamma receptor I (FcγRI; CD64) is the high-affinity receptor of the immunoglobulin G protein (IgG). It is usually expressed in immune cells and has recently been identified to distribute in the nervous system and play critical roles in various neurological disorders. Presently, the impacts of FcγRI in neuropathic pain was largely unknown. Here, we aimed to investigate the impacts of FcγRI in neuropathic pain through pain-related neurobehavioral studies and underlying mechanisms by biochemical methods in animal and cell models. Specifically, we first utilized the chronic constriction Injury (CCI) rat model that displayed neuropathic pain related symptoms and signs, including thermal hyperalgesia and mechanical allodynia. These neurobehavioral defects were significantly attenuated by the anti-FcγRI antibody, which was associated with reduced levels of neuropeptide substance P, C3, and TNF-α. Furthermore, we validated our animal findings using the embryonically neural crest-originated PC12 cell model. We found that stimulation of the IgG immune complex led to increased levels of FcγRI and inflammatory mediators, which were attenuated by the anti-FcγRI antibody in these cells. Collectively, our results from animal and cell-based studies suggest that FcγRI is a critical player for Peripheral Nerve Injury-induced neuropathic pain by mediating pain-related immunological events, which therefore may provide a new therapeutic target for protection against chronic pain.

  • necrostatin 1 ameliorates Peripheral Nerve Injury induced neuropathic pain by inhibiting the rip1 rip3 pathway
    Frontiers in Cellular Neuroscience, 2019
    Co-Authors: Yingxia Liang, Nannan Wang, Zhiyu Zhang, Zhaodong Juan, Can Zhang
    Abstract:

    Necrostatin-1 is an inhibitor of necroptosis, a form of programmed cell death that has been reported to be involved in various neurological diseases. Presently, the role of necroptosis in neuropathic pain induced by Peripheral Nerve Injury is still unclear. This study was focused on investigating the potential effects of necroptosis in the development and progression of neuropathic pain in a rat model and the possible neuroprotective effects of necrostatin-1 in neuropathic pain. The results indicated that the necroptosis-related proteins RIP1 and RIP3 significantly increased postoperation in the spinal cord in a neuropathic pain model and peaked 7 days postoperation, which was consistent with the time-dependent changes of hyperalgesia. Additionally, we found that Peripheral Nerve Injury-related behavioral and biochemical changes were significantly reduced by necrostatin-1. In particular, hyperalgesia was attenuated, and the levels of RIP1 and RIP3 were decreased. Furthermore, the ultrastructure of necrotic cell death and neuroinflammation were alleviated by necrostatin-1. Collectively, these results suggest that necroptosis is an important mechanism of cell death in neuropathic pain induced by Peripheral Nerve Injury and that necrostatin-1 may be a promising neuroprotective treatment for neuropathic pain.

Can Zhang - One of the best experts on this subject based on the ideXlab platform.

  • the high affinity igg receptor fcγri modulates Peripheral Nerve Injury induced neuropathic pain in rats
    Molecular Brain, 2019
    Co-Authors: Yingxia Liang, Zhiyu Zhang, Zhaodong Juan, Rui Zhang, Can Zhang
    Abstract:

    The Fc gamma receptor I (FcγRI; CD64) is the high-affinity receptor of the immunoglobulin G protein (IgG). It is usually expressed in immune cells and has recently been identified to distribute in the nervous system and play critical roles in various neurological disorders. Presently, the impacts of FcγRI in neuropathic pain was largely unknown. Here, we aimed to investigate the impacts of FcγRI in neuropathic pain through pain-related neurobehavioral studies and underlying mechanisms by biochemical methods in animal and cell models. Specifically, we first utilized the chronic constriction Injury (CCI) rat model that displayed neuropathic pain related symptoms and signs, including thermal hyperalgesia and mechanical allodynia. These neurobehavioral defects were significantly attenuated by the anti-FcγRI antibody, which was associated with reduced levels of neuropeptide substance P, C3, and TNF-α. Furthermore, we validated our animal findings using the embryonically neural crest-originated PC12 cell model. We found that stimulation of the IgG immune complex led to increased levels of FcγRI and inflammatory mediators, which were attenuated by the anti-FcγRI antibody in these cells. Collectively, our results from animal and cell-based studies suggest that FcγRI is a critical player for Peripheral Nerve Injury-induced neuropathic pain by mediating pain-related immunological events, which therefore may provide a new therapeutic target for protection against chronic pain.

  • necrostatin 1 ameliorates Peripheral Nerve Injury induced neuropathic pain by inhibiting the rip1 rip3 pathway
    Frontiers in Cellular Neuroscience, 2019
    Co-Authors: Yingxia Liang, Nannan Wang, Zhiyu Zhang, Zhaodong Juan, Can Zhang
    Abstract:

    Necrostatin-1 is an inhibitor of necroptosis, a form of programmed cell death that has been reported to be involved in various neurological diseases. Presently, the role of necroptosis in neuropathic pain induced by Peripheral Nerve Injury is still unclear. This study was focused on investigating the potential effects of necroptosis in the development and progression of neuropathic pain in a rat model and the possible neuroprotective effects of necrostatin-1 in neuropathic pain. The results indicated that the necroptosis-related proteins RIP1 and RIP3 significantly increased postoperation in the spinal cord in a neuropathic pain model and peaked 7 days postoperation, which was consistent with the time-dependent changes of hyperalgesia. Additionally, we found that Peripheral Nerve Injury-related behavioral and biochemical changes were significantly reduced by necrostatin-1. In particular, hyperalgesia was attenuated, and the levels of RIP1 and RIP3 were decreased. Furthermore, the ultrastructure of necrotic cell death and neuroinflammation were alleviated by necrostatin-1. Collectively, these results suggest that necroptosis is an important mechanism of cell death in neuropathic pain induced by Peripheral Nerve Injury and that necrostatin-1 may be a promising neuroprotective treatment for neuropathic pain.

Marzia Malcangio - One of the best experts on this subject based on the ideXlab platform.

  • role of spinal microglia in rat models of Peripheral Nerve Injury and inflammation
    European Journal of Pain, 2007
    Co-Authors: Anna K Clark, Clive Gentry, Elizabeth J Bradbury, Stephen B. Mcmahon, Marzia Malcangio
    Abstract:

    Mounting evidence supports the hypothesis that spinal microglia modulate the development and maintenance of some chronic pain states. Here we examined the role of spinal microglia following both Peripheral inflammatory insult and Peripheral Nerve Injury. We observed significant ipsilateral dorsal horn microglia activation 2 weeks after Injury and bilateral activation 50 days following Nerve Injury as well as 24 h following intraplantar zymosan but not intraplantar complete Freund's adjuvant (CFA). Ipsilateral but not contralateral microglia activation was associated with hind paw mechanical hyperalgesia. Spinal injection of the glial metabolic inactivator fluorocitrate attenuated ipsilateral hyperalgesia and bilateral spinal microglia activation after Peripheral Nerve Injury. Intrathecal fluorocitrate reversed hyperalgesia after intraplantar zymosan and produced no reversal of CFA-induced hyperalgesia. These data suggest a role for spinal glia in the persistence of mechanical hyperalgesia following Peripheral Nerve Injury. However, activation of spinal microglia contralaterally did not correlate to nociception. Furthermore, it would appear that the time course of microglia activation and their contribution to inflammatory pain is dependent on the inflammatory stimulus administered.

Nirmal Singh - One of the best experts on this subject based on the ideXlab platform.

  • role of different brain areas in Peripheral Nerve Injury induced neuropathic pain
    Brain Research, 2011
    Co-Authors: Amteshwar Singh Jaggi, Nirmal Singh
    Abstract:

    Neuropathic pain has been described as the "most terrible of all tortures which a Nerve wound may inflict" and arises as a consequence of Nerve Injury either of the Peripheral or central nervous system. Following Peripheral Nerve Injury, a cascade of events in the primary afferents leads to Peripheral sensitization resulting in spontaneous nociceptor activity, decreased threshold and increased response to supra-threshold stimuli. A series of molecular changes in spinal cord and brain centers are associated with central sensitization which is responsible for the pain to non-injured extra-territory regions (extraterritorial pain) and contralateral parts (mirror-image pain). The Peripheral Nerve Injury has been reported to induce neuroplastic changes in different brain regions including the anterior cingulate cortex, insular cortex, ventrolateral orbitofrontal area, amygdala, striatum, thalamus, hypothalamus, rostral ventromedial medulla, periaqueductal gray, pons (locus coeruleus), red nucleus, and medulla oblongata. The present review article discusses the involvement of these different brain areas in the development of Peripheral Nerve Injury-induced neuropathic pain.

Zhaodong Juan - One of the best experts on this subject based on the ideXlab platform.

  • the high affinity igg receptor fcγri modulates Peripheral Nerve Injury induced neuropathic pain in rats
    Molecular Brain, 2019
    Co-Authors: Yingxia Liang, Zhiyu Zhang, Zhaodong Juan, Rui Zhang, Can Zhang
    Abstract:

    The Fc gamma receptor I (FcγRI; CD64) is the high-affinity receptor of the immunoglobulin G protein (IgG). It is usually expressed in immune cells and has recently been identified to distribute in the nervous system and play critical roles in various neurological disorders. Presently, the impacts of FcγRI in neuropathic pain was largely unknown. Here, we aimed to investigate the impacts of FcγRI in neuropathic pain through pain-related neurobehavioral studies and underlying mechanisms by biochemical methods in animal and cell models. Specifically, we first utilized the chronic constriction Injury (CCI) rat model that displayed neuropathic pain related symptoms and signs, including thermal hyperalgesia and mechanical allodynia. These neurobehavioral defects were significantly attenuated by the anti-FcγRI antibody, which was associated with reduced levels of neuropeptide substance P, C3, and TNF-α. Furthermore, we validated our animal findings using the embryonically neural crest-originated PC12 cell model. We found that stimulation of the IgG immune complex led to increased levels of FcγRI and inflammatory mediators, which were attenuated by the anti-FcγRI antibody in these cells. Collectively, our results from animal and cell-based studies suggest that FcγRI is a critical player for Peripheral Nerve Injury-induced neuropathic pain by mediating pain-related immunological events, which therefore may provide a new therapeutic target for protection against chronic pain.

  • necrostatin 1 ameliorates Peripheral Nerve Injury induced neuropathic pain by inhibiting the rip1 rip3 pathway
    Frontiers in Cellular Neuroscience, 2019
    Co-Authors: Yingxia Liang, Nannan Wang, Zhiyu Zhang, Zhaodong Juan, Can Zhang
    Abstract:

    Necrostatin-1 is an inhibitor of necroptosis, a form of programmed cell death that has been reported to be involved in various neurological diseases. Presently, the role of necroptosis in neuropathic pain induced by Peripheral Nerve Injury is still unclear. This study was focused on investigating the potential effects of necroptosis in the development and progression of neuropathic pain in a rat model and the possible neuroprotective effects of necrostatin-1 in neuropathic pain. The results indicated that the necroptosis-related proteins RIP1 and RIP3 significantly increased postoperation in the spinal cord in a neuropathic pain model and peaked 7 days postoperation, which was consistent with the time-dependent changes of hyperalgesia. Additionally, we found that Peripheral Nerve Injury-related behavioral and biochemical changes were significantly reduced by necrostatin-1. In particular, hyperalgesia was attenuated, and the levels of RIP1 and RIP3 were decreased. Furthermore, the ultrastructure of necrotic cell death and neuroinflammation were alleviated by necrostatin-1. Collectively, these results suggest that necroptosis is an important mechanism of cell death in neuropathic pain induced by Peripheral Nerve Injury and that necrostatin-1 may be a promising neuroprotective treatment for neuropathic pain.