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Activation of GPR55 alleviates neuropathic pain and chronic inflammation.

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Title: Activation of GPR55 alleviates neuropathic pain and chronic inflammation.
Authors: Jiang, Weiqun1 (AUTHOR), Yu, Wenbin1 (AUTHOR) yu_wenbin05687@163.com, Tan, Yu1 (AUTHOR)
Source: Biotechnology & Applied Biochemistry. Feb2025, Vol. 72 Issue 1, p196-206. 11p.
Subjects: Laboratory rats, JAK-STAT pathway, Sciatic nerve, Neuralgia, Spinal cord, Glutathione peroxidase
Abstract: Neuropathic pain (NP) significantly impacts the quality of life due to its prolonged duration and lack of effective treatment. Recent findings suggest that targeting neuroinflammation is a promising approach for treating NP. G protein‐coupled receptor 55 (GPR55), a member of the GPCR family, plays an important role in neuroinflammatory regulation. CID16020046, a GPR55 agonist, possesses promising anti‐neuroinflammatory effects. Herein, the therapeutic effect of CID16020046 on NP was investigated in an NP rat model. The NP model was established using the unilateral sciatic nerve chronic constriction injury (CCI) assay. Both sham and CCI rats were intraperitoneally administered with 20 mg/kg CID16020046. NP was assessed using paw withdrawal threshold (PWT) and paw withdrawal latency (PWL). First, we showed that GPR55 was downregulated in the spinal dorsal horn of CCI rats. After CCI rats were treated with CID16020046, the values of PWT and PWL were increased, indicating their effect on pain relief. The treated rats had attenuated release of inflammatory cytokines in the spinal cord, decreased spinal malondialdehyde (MDA) levels, and increased spinal glutathione peroxidase (GSH‐PX) activity. Additionally, the increased levels of phosphorylated nuclear factor (NF)‐κB p65 in CCI rats were significantly alleviated by CID16020046 treatment. Mechanistically, we showed that CID16020046 significantly suppressed the activation of the Janus kinase (JAK2)/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway in the spinal cord of CCI‐treated rats. However, Colivelin TFA (a STAT3 agonist) abolished the effect of CID16020046 on JAK2/STAT3 activation. In conclusion, our data demonstrate that the activation of GPR55 by CID16020046 alleviates NP and neuroinflammation in CCI rats by mediating the JAK2/STAT3 pathway. [ABSTRACT FROM AUTHOR]
Copyright of Biotechnology & Applied Biochemistry is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Activation of GPR55 alleviates neuropathic pain and chronic inflammation.
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  Data: <searchLink fieldCode="AR" term="%22Jiang%2C+Weiqun%22">Jiang, Weiqun</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Yu%2C+Wenbin%22">Yu, Wenbin</searchLink><relatesTo>1</relatesTo> (AUTHOR)<i> yu_wenbin05687@163.com</i><br /><searchLink fieldCode="AR" term="%22Tan%2C+Yu%22">Tan, Yu</searchLink><relatesTo>1</relatesTo> (AUTHOR)
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  Data: <searchLink fieldCode="JN" term="%22Biotechnology+%26+Applied+Biochemistry%22">Biotechnology & Applied Biochemistry</searchLink>. Feb2025, Vol. 72 Issue 1, p196-206. 11p.
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  Data: <searchLink fieldCode="DE" term="%22Laboratory+rats%22">Laboratory rats</searchLink><br /><searchLink fieldCode="DE" term="%22JAK-STAT+pathway%22">JAK-STAT pathway</searchLink><br /><searchLink fieldCode="DE" term="%22Sciatic+nerve%22">Sciatic nerve</searchLink><br /><searchLink fieldCode="DE" term="%22Neuralgia%22">Neuralgia</searchLink><br /><searchLink fieldCode="DE" term="%22Spinal+cord%22">Spinal cord</searchLink><br /><searchLink fieldCode="DE" term="%22Glutathione+peroxidase%22">Glutathione peroxidase</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Neuropathic pain (NP) significantly impacts the quality of life due to its prolonged duration and lack of effective treatment. Recent findings suggest that targeting neuroinflammation is a promising approach for treating NP. G protein‐coupled receptor 55 (GPR55), a member of the GPCR family, plays an important role in neuroinflammatory regulation. CID16020046, a GPR55 agonist, possesses promising anti‐neuroinflammatory effects. Herein, the therapeutic effect of CID16020046 on NP was investigated in an NP rat model. The NP model was established using the unilateral sciatic nerve chronic constriction injury (CCI) assay. Both sham and CCI rats were intraperitoneally administered with 20 mg/kg CID16020046. NP was assessed using paw withdrawal threshold (PWT) and paw withdrawal latency (PWL). First, we showed that GPR55 was downregulated in the spinal dorsal horn of CCI rats. After CCI rats were treated with CID16020046, the values of PWT and PWL were increased, indicating their effect on pain relief. The treated rats had attenuated release of inflammatory cytokines in the spinal cord, decreased spinal malondialdehyde (MDA) levels, and increased spinal glutathione peroxidase (GSH‐PX) activity. Additionally, the increased levels of phosphorylated nuclear factor (NF)‐κB p65 in CCI rats were significantly alleviated by CID16020046 treatment. Mechanistically, we showed that CID16020046 significantly suppressed the activation of the Janus kinase (JAK2)/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway in the spinal cord of CCI‐treated rats. However, Colivelin TFA (a STAT3 agonist) abolished the effect of CID16020046 on JAK2/STAT3 activation. In conclusion, our data demonstrate that the activation of GPR55 by CID16020046 alleviates NP and neuroinflammation in CCI rats by mediating the JAK2/STAT3 pathway. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
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  Data: <i>Copyright of Biotechnology & Applied Biochemistry is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1002/bab.2656
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        Text: English
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        Type: general
      – SubjectFull: JAK-STAT pathway
        Type: general
      – SubjectFull: Sciatic nerve
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      – SubjectFull: Neuralgia
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      – SubjectFull: Spinal cord
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      – SubjectFull: Glutathione peroxidase
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    Titles:
      – TitleFull: Activation of GPR55 alleviates neuropathic pain and chronic inflammation.
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            NameFull: Jiang, Weiqun
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            NameFull: Yu, Wenbin
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              M: 02
              Text: Feb2025
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              Y: 2025
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