Evaluation of Armepavine Inhibiting LPS-Induced Inflammatory Cytokines Expression in Rat Mesangial Cells

Autor: Su De Shiuan, 蘇德軒
Rok vydání: 2006
Druh dokumentu: 學位論文 ; thesis
Popis: 94
According to the information from Department of Health, Executive Yuan, Taiwan, people died in nephropathy gradually increased. Glomerulonephritis is the most occurrence disease in all kinds of nephritis. Many studies indicate the pathogenesis of glomerulonephritis is related to immune complexes deposition, mesangial cells proliferation, and inflammatory cytokines overexpression such as interleukin-1β (IL-β), IL-6, and tumor necrosis factor-α (TNF-α). Moreover, some diseases including diabetes, hypertension, systemic lupus erythematosus, and upper respiratory tract infection often accompany glomerulonephritis. Previous studies indicate mesangial cells proliferation is one of the diagnostic markers of glomerulonephritis. Lipopolysaccharide (LPS) stimulated mesangial cells to release numerous inflammatory cytokines, such as IL-1β, IL-6, and TNF-α. They also secrete M-CSF and ICAM-1 to recruit macrophages. Our previous studies indicate that armepavine (C19H23O3N; MW313) purified from Nelumbo nucifera possesses immune modulatory functions. To evaluate the healing effects of armepavine on nephritis, the rat mesangial cells were applied as target cells, and effects of armepavine on inflammatory cytokines expression such as TNF-α and IL-6 were determined. The results demonstrated that LPS stimulated IL-6 and TNF-α mRNA expression in rat mesangial cells. However, armepavine decreased the levels of these transcripts in the cells with a dose-dependent manner. The results demonstrated that LPS stimulated TNF-α gene expression in rat mesangial cells by activation of mitogen-activated protein kinase (MAPK), NF-κB, and phosphoinositide 3-kinase (PI3K) pathways. The data proved that armepavine inhibited activation of MAPK, PI3K, and NF-κB in rat mesangial cells induced by LPS. Thus, we suggested that armepavine decreased TNF-α gene expression in rat mesangial cells through modulation of MAPK, NF-κB and PI3K activation.
Databáze: Networked Digital Library of Theses & Dissertations
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