ArticleOpen medicine (Warsaw, Poland)2022
Lidocaine ameliorates chronic constriction injury-induced neuropathic pain through regulating M1/M2 microglia polarization.
Article in Open medicine (Warsaw, Poland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Lidocaine alleviates diabetic neuropathic pain by inhibiting spinal astrocyte activation through modulation of the CXCL13/CXCR5 axis.Journal of molecular histology · 2026Article
- Microglia Polarization: A Key Regulatory Mechanism of Neuropathic Pain.Journal of pain research · 2026Review
- Temporal therapy utilizing exosomes derived from M2 macrophages demonstrates enhanced efficacy in alleviating neuropathic pain in diabetic rats.The Korean journal of pain · 2025Article
- GDPD3 Deficiency Alleviates Neuropathic Pain and Reprograms Macrophagic Polarization Through PGE2 and PPARγ Pathway.Neurochemical research · 2024Article
- Role of M1/M2 macrophages in pain modulation.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Review
- Article
- The N6-methyladenosine pattern of MAP3K7 mediates the effects of sevoflurane on macrophage M2 polarization and cervical cancer migration and invasion.Central-European journal of immunology · 2024Article
- Article
- Dual roles of anesthetics in postoperative cognitive dysfunction: Regulation of microglial activation through inflammatory signaling pathways.Frontiers in immunology · 2023Review
- Unraveling the emerging role of glial heterogeneity in neuropathic pain: from pathological mechanisms to therapeutic Frontiers.Frontiers in neurologyReview
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study is intended to explore the mechanism that lidocaine ameliorates chronic constriction injury (CCI)-induced neuropathic pain (NP) related to the polarization of M1 and M2 microglia. CCI rats were established by surgery to induce NP. The mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) of rats were determined. Microglial line HAPI cells were polarized into M1 or M2 cells using lipopolysaccharide (LPS) or interleukin (IL)-4, respectively. Immunofluorescence staining was performed to determine the Iba1/CD86- and Iba1/CD206-positive cells. Markers of M1 and M2 microglia were assessed using flow cytometry. Real-time polymerase chain reaction and enzyme-linked immunosorbent assay were performed to detect the level of mRNA and inflammatory factors. Lidocaine ameliorates CCI-induced NP, evidenced by the markedly increased values of MWT and TWL in NP rats. Lidocaine inhibited M1 microglia polarization but promoted M2 microglia polarization in a rat model of CCI-induced NP. Besides, in the
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