GLP-2 Attenuates LPS-Induced Inflammation in BV-2 Cells by Inhibiting ERK1/2, JNK1/2 and NF-κB Signaling Pathways
| Autor: | Ying-Jie Gao, Shoupeng Fu, Su-Nan Li, Juxiong Liu, Wen-Zhi Ren, Bo-Wen Liu, Wei Wang, Nan Li, Shi-Yao Xu, Yalong Zeng, Xuan Yan, Dianfeng Liu |
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| Jazyk: | angličtina |
| Rok vydání: | 2016 |
| Předmět: |
Lipopolysaccharides
0301 basic medicine Gene Expression Nitric Oxide Synthase Type II microglia NF-κB lcsh:Chemistry glucagon-like peptide-2 Parkinson’s disease MAPK chemistry.chemical_compound GTP-Binding Protein alpha Subunits Gs Glucagon-Like Peptide 2 Phosphorylation lcsh:QH301-705.5 Spectroscopy Cell Line Transformed Microglia NF-kappa B General Medicine Computer Science Applications Cell biology Nitric oxide synthase medicine.anatomical_structure Cytokines Inflammation Mediators medicine.symptom Signal transduction hormones hormone substitutes and hormone antagonists Signal Transduction endocrine system MAP Kinase Signaling System p38 mitogen-activated protein kinases Inflammation Biology Article Catalysis Inorganic Chemistry 03 medical and health sciences medicine Animals Mitogen-Activated Protein Kinase 9 Mitogen-Activated Protein Kinase 8 RNA Messenger Physical and Theoretical Chemistry Molecular Biology Organic Chemistry Neurotoxicity medicine.disease 030104 developmental biology chemistry lcsh:Biology (General) lcsh:QD1-999 Cyclooxygenase 2 Immunology biology.protein |
| Zdroj: | International Journal of Molecular Sciences; Volume 17; Issue 2; Pages: 190 International Journal of Molecular Sciences, Vol 17, Iss 2, p 190 (2016) International Journal of Molecular Sciences |
| ISSN: | 1422-0067 |
| DOI: | 10.3390/ijms17020190 |
| Popis: | The pathogenesis of Parkinson’s disease (PD) often involves the over-activation of microglia. Over-activated microglia could produce several inflammatory mediators, which trigger excessive inflammation and ultimately cause dopaminergic neuron damage. Anti-inflammatory effects of glucagon-like peptide-2 (GLP-2) in the periphery have been shown. Nonetheless, it has not been illustrated in the brain. Thus, in this study, we aimed to understand the role of GLP-2 in microglia activation and to elucidate the underlying mechanisms. BV-2 cells were pretreated with GLP-2 and then stimulated by lipopolysaccharide (LPS). Cells were assessed for the responses of pro-inflammatory enzymes (iNOS and COX-2) and pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α); the related signaling pathways were evaluated by Western blotting. The rescue effect of GLP-2 on microglia-mediated neurotoxicity was also examined. The results showed that GLP-2 significantly reduced LPS-induced production of inducible nitric oxide synthase (iNOS), cyclooxygenase-s (COX-2), IL-1β, IL-6 and TNF-α. Blocking of Gαs by NF449 resulted in a loss of this anti-inflammatory effect in BV-2 cells. Analyses in signaling pathways demonstrated that GLP-2 reduced LPS-induced phosphorylation of ERK1/2, JNK1/2 and p65, while no effect was observed on p38 phosphorylation. In addition, GLP-2 could suppress microglia-mediated neurotoxicity. All results imply that GLP-2 inhibits LPS-induced microglia activation by collectively regulating ERK1/2, JNK1/2 and p65. |
| Databáze: | OpenAIRE |
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