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논문분류	춘계학술대회 초록집
제목	p38 MAPK inhibitor attenuates fibrosis in unilateral ureteral obstruction mice model
저자	Jeonghwan Lee* 1, Jung Nam An2, Jin Hyuk Kim2, Jin Ho Hwang3, Seung Hee Yang4, Sung Gyun Kim5, Chun Soo Lim2, Yon Su Kim6, Jung Pyo Lee2
출판정보	2016; 2016(1):
키워드	chronic kidney disease, fibrosis, UUO
초록	Background: The p38 mitogen-activated protein kinases (MAPKs) release proinflammatory and vasoregulatory cytokines, and contribute renal inflammation. The p38 MAPKs are activated in the kidney fibrosis model. The role of p38 MAPKs in kidney fibrosis models are not fully evaluated. We investigated the effects of p38 MAPK inhibitors in the unilateral ureteral obstruction (UUO) model of mice. Methods: Renal fibrosis was induced by ligation of unilateral left ureter in male C57BL/6 (20g, 7-week old) mice. The p38 MAPK inhibitors (SB-731445) diluted in 20% DMSO were injected intraperitoneally for 7 days (dose: 0, 5, 10 mg/kg/day, n= 5 respectively). Results: Renal fibrosis was successfully introduced after ligation of unilateral ureter of mice. The expression of mRNAs associated with renal fibrosis, including αSMA (α smooth muscle actin), COL1 (type 1 collagen), fibronectin, was significantly decreased after administration of p38 MAPK inhibitors showing dose-dependency. Monocyte chemoattractant protein-1 (MCP-1) expression increased significantly after unilateral ureteral ligation, and decreased dose-dependently after p38 MAPK inhibitor treatment. Renal protein abundance of COL1 (29.7 ± 12.9%, 12.5 ± 8.6% of the control, P = 0.04) and p53 (80.8 ± 7.4%, 37.1 ± 19.3% of the control, P = 0.03) decreased significantly after 1 week treatment of p38 MAPK inhibitor 5 and 10 mg/kg/day, respectively. Conclusion: Activities of p38 MAPKs are increased in the pathogenesis of renal fibrosis. Inhibitors of p38 MAPKs can suppress the expression of mRNAs associated with renal fibrosis and inflammation, and decrease the renal abundance of COL1 in UUO chronic kidney disease mice model. Figures:
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