miR‐98 acts as an inhibitor in chronic constriction injury‐induced neuropathic pain via downregulation of high‐mobility group AT‐hook 2

2019 ◽  
Vol 120 (6) ◽  
pp. 10363-10369 ◽  
Author(s):  
Yang Zhang ◽  
Zhen Su ◽  
Li‐Jun An ◽  
Lin Li ◽  
Meng Wei ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Chronic Constriction Injury ◽  
High Mobility ◽  
High Mobility Group

scholarly journals Intrathecal Lentivirus-mediated Transfer of Interleukin-10 Attenuates Chronic Constriction Injury-induced Neuropathic Pain through Modulation of Spinal High-mobility Group Box 1 in Rats

2013 ◽  
Vol 5;16 (5;9) ◽  
pp. E615-E625
Author(s):  
Wangyuan Zou
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Rat Model ◽  
Inflammatory Markers ◽  
Chronic Constriction Injury ◽  
High Mobility ◽  
Interleukin 10 ◽  
High Mobility Group ◽  
Control Vector ◽  
Tnf Α

Background: Neuropathic pain is a complex state of chronic pain that is usually accompanied by peripheral and central nervous system damage or dysfunction. Previous studies have indicated that neuroinflammation in the spinal cord is an important contributor to neuropathological and behavioral abnormalities. A series of early inflammatory markers, such as IL-1, TNF-α, and IFN-γ, and advanced inflammatory markers, such as high-mobility group box 1 (HMGB1), are involved in neuroinflammation. Study Design: A randomized, double blind, controlled animal trial. Objective: In this study, a lentivirus delivering human IL-10 (LV/hIL-10) was administered intrathecally to determine the effects of IL-10 on allodynia and hyperalgesia in a chronic constriction injury-induced (CCI) rat model of neuropathic pain. Methods: Sprague-Dawley rats weighting 260 - 320 g were randomly divided into 4 groups. Group Sham (Sham), Group CCI±Normal Saline (NS), Group CCI±LV/hIL-10 (LV/hIL-10), and Group CCI±LV/control (vector). Rats in each group were intrathecally administered NS, LV/control, or recombinant vector LV/hIL-10 in a total volume of 10 μl. Paw withdrawal mechanical thresholds (PWMT) and paw withdrawal thermal latency PWTL were measured one day before CCI (baseline) and 0, 3, 7, 14, and 28 days after intrathecal administration. Cerebrospinal fluid (CSF) samples were collected during surgical plane anesthesia and the collected CSF samples were used to assay for human IL-10, rat IL-1β, rat IL-6, and rat TNF-α by enzyme-linked immunosorbent assay (ELISA). Animals were sacrificed and the L4-5 lumbar segment of the spinal cord was removed for determination of green fluorescent protein (GFP) expression. Immunohistochemical analysis was performed using anti HMGB1 antibodies and the expression of HMGB1 protein in the spinal cord was determined by Western blot analysis after intrathecal delivery (n = 8 each). Results: The results show that intrathecal LV/hIL-10 reverses enhanced pain states. Moreover, the increased level of HMGB1 exhibited in a late stage of CCI was inhibited by exogenous overexpression of hIL-10 in the CCI model. Expression of HMGB1, RAGE, and pAkt were lower in CCI-induced rats treated with LV/hIL-10 than in those treated with LV/control (vector) or saline (NS). Our results showed that IL-10 inhibits activation of the inflammatory HMGB1-RAGE pathway in the CCI rat model. Limitations: Further experimental investigations are needed to clarify the specific biological roles played by HMGB1 in IL-10-mediated regulation of neuropathic pain. Conclusion: Our results indicate that intrathecal lentiviral-mediated transfer of IL-10 attenuates CCI-induced neuropathic pain in rats. The anti-thermal hyperalgesia and anti-mechanical allodynia may be partly attributable to the decreased expression of HMGB1 and inhibition of HMGB1-RAGE pathway. Key words: Analgesia, interleukin-10, lentiviral, HMGB1, intrathecal, randomized, controlled trial

scholarly journals MicroRNA-142-3p relieves neuropathic pain by targeting high mobility group box 1

2017 ◽  
Author(s):  
Yang Zhang ◽  
Junying Mou ◽  
Li Cao ◽  
Su Zhen ◽  
Hongjuan Huang ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
High Mobility ◽  
High Mobility Group

scholarly journals Neuropathic Pain in Rats with a Partial Sciatic Nerve Ligation Is Alleviated by Intravenous Injection of Monoclonal Antibody to High Mobility Group Box-1

PLoS ONE ◽  
2013 ◽  
Vol 8 (8) ◽  
pp. e73640 ◽  
Author(s):  
Yoki Nakamura ◽  
Norimitsu Morioka ◽  
Hiromi Abe ◽  
Fang Fang Zhang ◽  
Kazue Hisaoka-Nakashima ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Neuropathic Pain ◽  
Sciatic Nerve ◽  
Intravenous Injection ◽  
High Mobility ◽  
High Mobility Group ◽  
Partial Sciatic Nerve Ligation

High-mobility group box 1-mediated microglial activation induces anxiodepressive-like behaviors in mice with neuropathic pain

2019 ◽  
Vol 92 ◽  
pp. 347-362 ◽  
Author(s):  
Kazue Hisaoka-Nakashima ◽  
Yoshiaki Tomimura ◽  
Toshiki Yoshii ◽  
Kazuto Ohata ◽  
Naoki Takada ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Microglial Activation ◽  
High Mobility ◽  
High Mobility Group

scholarly journals Pretreatment with High Mobility Group Box-1 Monoclonal Antibody Prevents the Onset of Trigeminal Neuropathy in Mice with a Distal Infraorbital Nerve Chronic Constriction Injury

Molecules ◽  
2021 ◽  
Vol 26 (7) ◽  
pp. 2035
Author(s):  
Takahiro Kochi ◽  
Yoki Nakamura ◽  
Simeng Ma ◽  
Kazue Hisaoka-Nakashima ◽  
Dengli Wang ◽  
...  
Keyword(s):  
Nerve Injury ◽  
Trigeminal Nerve ◽  
Immune Cells ◽  
Cell Activation ◽  
Chronic Constriction Injury ◽  
Immune Cell ◽  
Tissue Injury ◽  
High Mobility ◽  
High Mobility Group ◽  
Infraorbital Nerve

Persistent pain following orofacial surgery is not uncommon. High mobility group box 1 (HMGB1), an alarmin, is released by peripheral immune cells following nerve injury and could be related to pain associated with trigeminal nerve injury. Distal infraorbital nerve chronic constriction injury (dIoN-CCI) evokes pain-related behaviors including increased facial grooming and hyper-responsiveness to acetone (cutaneous cooling) after dIoN-CCI surgery in mice. In addition, dIoN-CCI mice developed conditioned place preference to mirogabalin, suggesting increased neuropathic pain-related aversion. Treatment of the infraorbital nerve with neutralizing antibody HMGB1 (anti-HMGB1 nAb) before dIoN-CCI prevented both facial grooming and hyper-responsiveness to cooling. Pretreatment with anti-HMGB1 nAb also blocked immune cell activation associated with trigeminal nerve injury including the accumulation of macrophage around the injured IoN and increased microglia activation in the ipsilateral spinal trigeminal nucleus caudalis. The current findings demonstrated that blocking of HMGB1 prior to nerve injury prevents the onset of pain-related behaviors, possibly through blocking the activation of immune cells associated with the nerve injury, both within the CNS and on peripheral nerves. The current findings further suggest that blocking HMGB1 before tissue injury could be a novel strategy to prevent the induction of chronic pain following orofacial surgeries.

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