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EPO prevents neuroinflammation and relieves depression via JAK/STAT signaling.
Luo, Yanhua; Ali, Tahir; Liu, Zizhen; Gao, Ruyan; Li, Axiang; Yang, Canyu; Ling, Li; He, Liufang; Li, Shupeng.
Afiliación
  • Luo Y; State Key Laboratory of Chemical Oncogenomics, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen 518055, China. Electronic address: 2001212649@stu.pku.edu.cn.
  • Ali T; State Key Laboratory of Chemical Oncogenomics, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen 518055, China; Institute of Chemical Biology, Shenzhen Bay Laboratory, Shenzhen 518132, China. Electronic address: tali@bs.qau.edu.pk.
  • Liu Z; State Key Laboratory of Chemical Oncogenomics, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen 518055, China. Electronic address: ZzLiu@pku.edu.cn.
  • Gao R; State Key Laboratory of Chemical Oncogenomics, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen 518055, China. Electronic address: gaoruyan@pku.edu.cn.
  • Li A; Institute of Forensic Injury, Institute of Forensic Bio-Evidence, Western China Science and Technology Innovation Harbor, Xi'an Jiaotong University, Xi'an, China. Electronic address: liaxiang5045@stu.xjtu.edu.cn.
  • Yang C; Institute of Forensic Injury, Institute of Forensic Bio-Evidence, Western China Science and Technology Innovation Harbor, Xi'an Jiaotong University, Xi'an, China. Electronic address: yangcanyu1996@stu.xjtu.edu.cn.
  • Ling L; Department of Endocrinology, The 6th Affiliated Hospital of Shenzhen University Medical School and Huazhong University of Science and Technology Union Shenzhen Hospital, Shenzhen, China. Electronic address: lingli2018@email.szu.edu.cn.
  • He L; Pediatrics Department, Shenzhen University General Hospital, Shenzhen University, Shenzhen, China. Electronic address: heliufang6022@163.com.
  • Li S; State Key Laboratory of Chemical Oncogenomics, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen 518055, China; Institute of Chemical Biology, Shenzhen Bay Laboratory, Shenzhen 518132, China; Department of Psychiatry, University of Toronto, Toronto, O
Life Sci ; 333: 122102, 2023 Nov 15.
Article en En | MEDLINE | ID: mdl-37769806
AIMS: Erythropoietin (EPO) is a glycoprotein cytokine that exerts therapeutic potential on neurological disorders by promoting neurogenesis and angiogenesis. However, its role as an antidepressant via anti-inflammatory axes is poorly explored. Furthermore, chronic inflammation can induce neuroinflammation, concurrent with depressive-like behaviors that anti-inflammatory and antidepressant agents could avert. Here, we aimed to elucidate the antidepressant potential of Erythropoietin (EPO) in the LPS-induced depression model. MAIN METHODS: For in vivo analysis, mice were treated with LPS (2 mg/kg BW), Erythropoietin (EPO) (5000 U/kg/day), (Ruxolitinib,15 mg/kg), and K252a (25 µg/kg). Depressive-like behaviors were confirmed via behavior tests, including OFT, FST, SPT, and TST. Cytokines were measured via ELISA, while IBA-1/GFAP expression was determined by immunofluorescence. Further, the desired gene expression was measured by immunoblotting. For in vitro analysis, BV2 and N2a cell lines were cultured, treated with LPS, EPO, Ruxolitinib, and K252a, collected, and analyzed. KEY FINDINGS: LPS treatment significantly induced neuroinflammation accompanied by depression-like behaviors in mice. However, EPO treatment rescued LPS-induced changes by averting cytokine production, secretion, and glial cell activation and reducing depressive-like behaviors in mice. Surprisingly, EPO treatment ameliorated LPS-induced JAK2/STAT5 signaling impairment, as validated by JAK2-antagonism. Furthermore, synaptic and dendritic spine defects and BNDF/TrkB signaling upon LPS administration could be prevented by EPO treatment. SIGNIFICANCE: EPO could act as an antidepressant via its anti-inflammatory potential by regulating JAK2/STAT5 signaling.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Eritropoyetina / Factor de Transcripción STAT5 Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Life Sci Año: 2023 Tipo del documento: Article Pais de publicación: Países Bajos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Eritropoyetina / Factor de Transcripción STAT5 Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Life Sci Año: 2023 Tipo del documento: Article Pais de publicación: Países Bajos