Electroacupuncture Alleviates Experimental Chronic Inflammatory Pain by Inhibiting Calcium Voltage-Gated Channel-Mediated Inflammation
Autor: | Zhou Jie, You Zhou, Ying Jin, Rui-Jie Ma, Yi Liang, Qin Chen, Jianqiao Fang, Hongyun Song, Yueyang Chai |
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Rok vydání: | 2019 |
Předmět: |
0303 health sciences
Article Subject Chemistry Pharmacology Serotonergic Transcriptome Synapse Other systems of medicine 03 medical and health sciences 0302 clinical medicine Complementary and alternative medicine Downregulation and upregulation Glutamatergic synapse Cholinergic synapse KEGG Signal transduction RZ201-999 030217 neurology & neurosurgery 030304 developmental biology Research Article |
Zdroj: | Evidence-based Complementary and Alternative Medicine : eCAM Evidence-Based Complementary and Alternative Medicine, Vol 2020 (2020) |
ISSN: | 1741-427X |
Popis: | Background. Both experimental and clinical studies have shown that electroacupuncture (EA) administration ameliorates chronic inflammatory pain (CIP). However, the multifaceted mechanism underlying the effects of EA on CIP is poorly understood. In this study, the mRNA transcriptome was used to study various therapeutic targets of EA. Methods. Using RNA-sequencing, protein-coding mRNA expression profiles of the L4-L5 dorsal root ganglion (DRG) were examined in the control (CN), complete Freund’s adjuvant- (CFA-) induced CIP, and EA-treated CIP groups. A series of bioinformatics analyses was performed; “EA-reversed upregulated genes with CIP” (up-DEGs) and “EA-reversed downregulated genes with CIP” (down-DEGs) were identified. Thereafter, based on up-DEGs and down-DEGs, biological functions and signaling pathways were enriched using gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) pathway analyses. Results. In total, 189 DEGs were identified, including 134 up- and 55 down-DEGs, which were enriched in arachidonic acid metabolism (rno00590), glutamatergic synapse (rno04724), serotonergic synapse (rno04726), FoxO signaling pathway (rno04068), insulin signaling pathway (rno04910), amyotrophic lateral sclerosis (rno05014), cholinergic synapse (rno04725), ECM-receptor interaction (rno04512), and choline metabolism in cancer (rno05231). Conclusion. We identified a few GOs, pathways, and genes that could play key roles in the amelioration of CIP by EA. Hence, this study may provide a theoretical basis for CIP amelioration by EA. |
Databáze: | OpenAIRE |
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