Chinese Angelica Polysaccharide (CAP) Alleviates LPS-Induced Inflammation and Apoptosis by Down-Regulating COX-1 in PC12 Cells
Autor: | Hai-Tao Zhang, Zheng Wang, Yun-Jie Xie, Deyi Duan, Yang Zhang, Chong Wang |
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Rok vydání: | 2018 |
Předmět: |
Lipopolysaccharides
0301 basic medicine Angelica sinensis Physiology Interleukin-1beta Cell Down-Regulation Apoptosis Spinal cord injury Chinese angelica polysaccharide PC12 Cells lcsh:Physiology lcsh:Biochemistry Phosphatidylinositol 3-Kinases 03 medical and health sciences 0302 clinical medicine Western blot Polysaccharides medicine Animals lcsh:QD415-436 Viability assay Medicine Chinese Traditional Cell damage PI3K/AKT/mTOR pathway Angelica bcl-2-Associated X Protein Inflammation lcsh:QP1-981 medicine.diagnostic_test biology COX-1 Caspase 3 Interleukin-6 Tumor Necrosis Factor-alpha Chemistry Transfection biology.organism_classification medicine.disease Rats Cell biology 030104 developmental biology medicine.anatomical_structure Proto-Oncogene Proteins c-bcl-2 030220 oncology & carcinogenesis Cyclooxygenase 1 Proto-Oncogene Proteins c-akt Signal Transduction |
Zdroj: | Cellular Physiology and Biochemistry, Vol 49, Iss 4, Pp 1380-1388 (2018) |
ISSN: | 1421-9778 1015-8987 |
DOI: | 10.1159/000493415 |
Popis: | Background/Aims: Chinese angelica polysaccharide (CAP) is the main effective ingredient of angelica sinensis and exerts anti-inflammatory and anti-apoptotic effects on many diseases. This study aimed to explore the pharmacological potential of CAP on spinal cord injury (SCI). Methods: PC12 cells were pretreated by CAP and were subjected to LPS. Transfection was performed to alter the expression of COX-1. Cell viability and apoptotic cell rate were measured by CCK-8 and flow cytometry respectively. qRT-PCR and western blot analysis were performed to assess the expression changes of pro-inflammatory cytokines, apoptosis-related factor and core kinases in PI3K/AKT pathway. Results: LPS stimulation induced significant cell damage in PC12 cells as cell viability was repressed, apoptosis was induced and the expression levels of IL-1β, IL-6, IL-8, and TNF-α were increased. CAP pretreatment protected PC12 cells against LPS-induced cell damage. Meanwhile CAP treatment reduced the expression of COX-1 even in LPS-stimulated PC12 cells. More importantly, COX-1 overexpression abolished the protective effects of CAP on LPS-injured PC12 cells. Finally, Western blot analytical results showed that CAP activated PI3K/AKT pathway also in a COX-1-dependent manner. Conclusion: CAP exerted anti-apoptotic and anti-inflammatory effects on LPS-injured PC12 cells via down-regulation of COX-1. |
Databáze: | OpenAIRE |
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