International immunopharmacology · 2024
Isoliquiritigenin alleviates neuropathic pain by reducing microglia inflammation through inhibition of the ERK signaling pathway and decreasing CEBPB transcription expression.
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Wang Zikun, Jia Shu, Kang Xizhi, Chen Shang, Zhang Lu, Tian ZhiKang, Liang Xiao, Meng Chunyang
Аннотация
BACKGROUND: Natural compounds are invaluable for their therapeutic effects in treating various diseases. Isoliquiritigenin (ISL) stands out due to its potent anti-inflammatory and antioxidative properties, offering significant therapeutic effects in many diseases. However, there is currently no existing literature on the role of ISL in neuropathic pain treatment.
METHODS: We used lipopolysaccharide to stimulate BV-2 microglia in order to evaluate the inhibitory effects of ISL on neuroinflammation. Proteomics data and protein-protein interaction network analysis were used to identify differential proteins expressed in BV-2 microglia treated with ISL. This allowed for the identification of targets impacted by ISL action. Additionally, we assessed the analgesic efficacy of ISL in a mouse model of chronic constriction injury of the sciatic nerve (CCI) and investigated its inhibitory influence on pro-inflammatory cytokine production and spinal microglia activation.
RESULTS: Our results indicate that ISL efficiently inhibits BV-2 microglia activation and pro-inflammatory cytokine expression. Furthermore, CEBPB has been recognized as a possible target for ISL activity. Crucially, microglia activation was successfully reduced by CEBPB knockdown. Functional recovery tests carried out later on validated that ISL works by specifically inhibiting the ERK/CEBPB signaling pathway. In vivo studies showed that giving mice ISL reduces the mechanical and thermal pain caused on by chronic contraction injuries.
CONCLUSION: The analgesic effect of ISL on neuropathic pain primarily stems from its ability to inhibit the activation of spinal microglia and neuroinflammation. This mechanism may be attributed to the capacity of ISL to suppress microglial activation, reduce the expression of pro-inflammatory cytokines by inhibiting the ERK signaling pathway, and decrease transcriptional expression of CEBPB.
METHODS: We used lipopolysaccharide to stimulate BV-2 microglia in order to evaluate the inhibitory effects of ISL on neuroinflammation. Proteomics data and protein-protein interaction network analysis were used to identify differential proteins expressed in BV-2 microglia treated with ISL. This allowed for the identification of targets impacted by ISL action. Additionally, we assessed the analgesic efficacy of ISL in a mouse model of chronic constriction injury of the sciatic nerve (CCI) and investigated its inhibitory influence on pro-inflammatory cytokine production and spinal microglia activation.
RESULTS: Our results indicate that ISL efficiently inhibits BV-2 microglia activation and pro-inflammatory cytokine expression. Furthermore, CEBPB has been recognized as a possible target for ISL activity. Crucially, microglia activation was successfully reduced by CEBPB knockdown. Functional recovery tests carried out later on validated that ISL works by specifically inhibiting the ERK/CEBPB signaling pathway. In vivo studies showed that giving mice ISL reduces the mechanical and thermal pain caused on by chronic contraction injuries.
CONCLUSION: The analgesic effect of ISL on neuropathic pain primarily stems from its ability to inhibit the activation of spinal microglia and neuroinflammation. This mechanism may be attributed to the capacity of ISL to suppress microglial activation, reduce the expression of pro-inflammatory cytokines by inhibiting the ERK signaling pathway, and decrease transcriptional expression of CEBPB.