Guihua Tian, Meiyue Wang, Ke He, Xinyi Li, Yang Wu, Huifeng Hao, Fan Zhang, Youxiang Su, Junyi Long, Yi Lin, Zhihao Shang, Liangqing Huang
{"title":"电针通过抑制LncRNA meg3介导的Wnt/β-Catenin信号通路改善CPSP大鼠神经炎症损伤","authors":"Guihua Tian, Meiyue Wang, Ke He, Xinyi Li, Yang Wu, Huifeng Hao, Fan Zhang, Youxiang Su, Junyi Long, Yi Lin, Zhihao Shang, Liangqing Huang","doi":"10.1007/s11064-025-04547-z","DOIUrl":null,"url":null,"abstract":"<div><p>Electroacupuncture (EA) therapy has been shown to significantly alleviate central poststroke pain (CPSP). However, current research on the mechanisms by which EA relieves CPSP is insufficient. This study explored the role of EA in ameliorating central nervous system inflammation in CPSP rats.The CPSP rat model was established by injecting collagenase IV into the right ventral posterolateral nucleus of the thalamus (VPL). The treatment group was treated with 15 Hz and 2 mA continuous wave EA every other day for a total of 8 sessions. The lncRNA MEG3 (MEG3) was knocked down or overexpressed by adeno-associated virus delivery in vivo in the rat brain. Pain thresholds were measured to assess the hypersensitivity of the rats to pain. Immunofluorescence, Nissl staining and enzyme-linked immunosorbent assay (ELISA) were used to assess the levels of <i>MEG3</i> and glial fibrillary acidic protein (GFAP) in VPL brain tissue, neuronal injury, and the levels of substance P (SP), TNF-α, IL-1β and IL-6 in VPL brain tissue and serum, respectively. The levels of <i>MEG3</i>, Wnt3a, β-catenin and GFAP in VPL brain tissue were assessed by qRT‒PCR or Western blotting. EA inhibits the expression of <i>MEG3</i> and neuroinflammatory injury in the VPL brain tissue of CPSP rats, ameliorating hyperalgesia symptoms in CPSP rats. The overexpression of <i>MEG3</i> weakened the inhibitory effect of EA on the Wnt/β-catenin pathway in the VPL region of the brain, exacerbating pain hypersensitivity and neuroinflammatory damage in the brain hemorrhage regions of CPSP rats. Suppressing the expression of <i>MEG3</i> in the VPL brain tissue of CPSP rats produced a therapeutic effect similar to that of EA intervention. EA could alleviate neuroinflammation and reduce pain in CPSP rats by suppressing the expression of <i>MEG3</i>. EA could regulate the Wnt/β-catenin signaling pathway via <i>MEG3</i>.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 5","pages":""},"PeriodicalIF":3.8000,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s11064-025-04547-z.pdf","citationCount":"0","resultStr":"{\"title\":\"Electroacupuncture Ameliorates Neuroinflammatory Injury in CPSP Rats by Inhibiting the LncRNA MEG3-Mediated Wnt/β-Catenin Signaling Pathway\",\"authors\":\"Guihua Tian, Meiyue Wang, Ke He, Xinyi Li, Yang Wu, Huifeng Hao, Fan Zhang, Youxiang Su, Junyi Long, Yi Lin, Zhihao Shang, Liangqing Huang\",\"doi\":\"10.1007/s11064-025-04547-z\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Electroacupuncture (EA) therapy has been shown to significantly alleviate central poststroke pain (CPSP). However, current research on the mechanisms by which EA relieves CPSP is insufficient. This study explored the role of EA in ameliorating central nervous system inflammation in CPSP rats.The CPSP rat model was established by injecting collagenase IV into the right ventral posterolateral nucleus of the thalamus (VPL). The treatment group was treated with 15 Hz and 2 mA continuous wave EA every other day for a total of 8 sessions. The lncRNA MEG3 (MEG3) was knocked down or overexpressed by adeno-associated virus delivery in vivo in the rat brain. Pain thresholds were measured to assess the hypersensitivity of the rats to pain. Immunofluorescence, Nissl staining and enzyme-linked immunosorbent assay (ELISA) were used to assess the levels of <i>MEG3</i> and glial fibrillary acidic protein (GFAP) in VPL brain tissue, neuronal injury, and the levels of substance P (SP), TNF-α, IL-1β and IL-6 in VPL brain tissue and serum, respectively. The levels of <i>MEG3</i>, Wnt3a, β-catenin and GFAP in VPL brain tissue were assessed by qRT‒PCR or Western blotting. EA inhibits the expression of <i>MEG3</i> and neuroinflammatory injury in the VPL brain tissue of CPSP rats, ameliorating hyperalgesia symptoms in CPSP rats. The overexpression of <i>MEG3</i> weakened the inhibitory effect of EA on the Wnt/β-catenin pathway in the VPL region of the brain, exacerbating pain hypersensitivity and neuroinflammatory damage in the brain hemorrhage regions of CPSP rats. Suppressing the expression of <i>MEG3</i> in the VPL brain tissue of CPSP rats produced a therapeutic effect similar to that of EA intervention. EA could alleviate neuroinflammation and reduce pain in CPSP rats by suppressing the expression of <i>MEG3</i>. 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Electroacupuncture Ameliorates Neuroinflammatory Injury in CPSP Rats by Inhibiting the LncRNA MEG3-Mediated Wnt/β-Catenin Signaling Pathway
Electroacupuncture (EA) therapy has been shown to significantly alleviate central poststroke pain (CPSP). However, current research on the mechanisms by which EA relieves CPSP is insufficient. This study explored the role of EA in ameliorating central nervous system inflammation in CPSP rats.The CPSP rat model was established by injecting collagenase IV into the right ventral posterolateral nucleus of the thalamus (VPL). The treatment group was treated with 15 Hz and 2 mA continuous wave EA every other day for a total of 8 sessions. The lncRNA MEG3 (MEG3) was knocked down or overexpressed by adeno-associated virus delivery in vivo in the rat brain. Pain thresholds were measured to assess the hypersensitivity of the rats to pain. Immunofluorescence, Nissl staining and enzyme-linked immunosorbent assay (ELISA) were used to assess the levels of MEG3 and glial fibrillary acidic protein (GFAP) in VPL brain tissue, neuronal injury, and the levels of substance P (SP), TNF-α, IL-1β and IL-6 in VPL brain tissue and serum, respectively. The levels of MEG3, Wnt3a, β-catenin and GFAP in VPL brain tissue were assessed by qRT‒PCR or Western blotting. EA inhibits the expression of MEG3 and neuroinflammatory injury in the VPL brain tissue of CPSP rats, ameliorating hyperalgesia symptoms in CPSP rats. The overexpression of MEG3 weakened the inhibitory effect of EA on the Wnt/β-catenin pathway in the VPL region of the brain, exacerbating pain hypersensitivity and neuroinflammatory damage in the brain hemorrhage regions of CPSP rats. Suppressing the expression of MEG3 in the VPL brain tissue of CPSP rats produced a therapeutic effect similar to that of EA intervention. EA could alleviate neuroinflammation and reduce pain in CPSP rats by suppressing the expression of MEG3. EA could regulate the Wnt/β-catenin signaling pathway via MEG3.
期刊介绍:
Neurochemical Research is devoted to the rapid publication of studies that use neurochemical methodology in research on nervous system structure and function. The journal publishes original reports of experimental and clinical research results, perceptive reviews of significant problem areas in the neurosciences, brief comments of a methodological or interpretive nature, and research summaries conducted by leading scientists whose works are not readily available in English.