Glucosamine inhibits LPS-induced COX-2 and iNOS expression in mouse macrophage cells (RAW 264.7) by inhibition of p38-MAP kinase and transcription factor NF-κB

2007 ◽  
Vol 51 (5) ◽  
pp. 587-593 ◽  
Author(s):  
Mohamed M. Rafi ◽  
Prem N. Yadav ◽  
Andrea O. Rossi
2008 ◽  
Vol 22 (8) ◽  
pp. 1030-1034 ◽  
Author(s):  
Soo-Youn Choi ◽  
Joon-Ho Hwang ◽  
Soo-Young Park ◽  
Yeong-Jun Jin ◽  
Hee-Chul Ko ◽  
...  

2017 ◽  
Vol 2 (4) ◽  
pp. 523-531 ◽  
Author(s):  
Md Shafiqul Islam ◽  
Hideki Ushio ◽  
Masatoshi Hori ◽  
Hiroshi Ozaki

Cycloartenyl ferulate (CAF) is a major bioactive phytosteryl ferulate purified from rice bran ?- oryzanol. Previously we reported that CAF ameliorates DSS-induced colitis in mice. The present study was undertaken to investigate the effects of CAF on LPS (lipopolysaccharide) stimulated murine RAW 264.7 macrophages. Immunohistochemistry analysis demonstrated that LPS (10ng/mL) treatment exhibited nuclear translocation of NF-?B-p65 in RAW macrophages, which was markedly inhibited CAF (30?M). LPS (10ng/mL) stimulation for 1-4 hours significantly upregulated iNOS and COX-2 mRNA in RAW 264.7 macrophages, but COX-2 mRNA was faster than that of iNOS mRNA. Macrophages pretreated with CAF greatly inhibited the LPS stimulated iNOS mRNA in a dose dependent manner (1-30?M), but CAF weakly inhibited COX-2 mRNA. Interestingly, CAY 10404 (COX-2 inhibitor) inhibited LPS stimulated iNOS mRNA, but not COX-2. In addition, PGE2 (1?M) upregulated iNOS mRNA but did not show any remarkable effects on NF-?B-p65 nuclear translocation in RAW macrophages. PD98059 (p44/42 MAP kinase inhibitor) inhibited iNOS mRNA, but not COX-2. On the other hand, PD169316 (p38 MAP kinase inhibitor) neither inhibited iNOS mRNA nor COX-2. Our results suggest that iNOS mRNA expression by LPS is mediated via p44/42 MAP kinase pathway in RAW 264.7 macrophages, which depends on the preceding expression of COX-2 expression. CAF downregulates iNOS mRNA via an inhibition of nuclear translocation of NF-?B with different mode of action on COX-2 gene expression.Asian J. Med. Biol. Res. December 2016, 2(4): 523-531


2009 ◽  
Vol 31 (1) ◽  
pp. 103-107 ◽  
Author(s):  
Chikatoshi Kasugai ◽  
Akiko Morikawa ◽  
Yoshikazu Naiki ◽  
Naoki Koide ◽  
Takayuki Komatsu ◽  
...  

2004 ◽  
Vol 286 (4) ◽  
pp. F693-F701 ◽  
Author(s):  
Louis C. Martineau ◽  
Lyne I. McVeigh ◽  
Bernard J. Jasmin ◽  
Chris R. J. Kennedy

A dynamic cytoskeleton allows podocytes to withstand significant mechanical stress on elevation of intraglomerular capillary pressure (Pgc). However, vasoactive hormones, such as prostaglandin E2 (PGE2), may challenge the integrity of the actin cytoskeleton, alter podocyte morphology, and compromise glomerular permeability. PGE2 synthesis correlates with the onset of proteinuria and increased Pgc following reduced nephron mass. We investigated the interplay among mechanical stress, cyclooxygenase (COX), E-prostanoid (EP) receptor expression, and the actin cytoskeleton, using an in vitro model of cell stretch. Immortalized mouse podocytes grown on flexible silicone membranes were cyclically stretched (5% elongation, 0.5 Hz) for 2 h. EP4 and COX-2 mRNA increased three- and sevenfold above nonstretched controls, whereas EP1 and COX-1 levels were unchanged. Six hours of stretch resulted in a threefold increase in PGE2-stimulated cAMP accumulation, a measure of EP4 receptor function, and an increase in COX-2 protein. The stretch-induced effects on COX-2/EP4 expression and EP4-induced cAMP production were attributable to p38 MAP kinase, as blockade of this pathway, but not of ERK or JNK, abrogated the response. These stretch-induced changes in expression were transcriptionally dependent as they were actinomycin D sensitive. Finally, we investigated the influence of enhanced EP4 signaling on the actin cytoskeleton. Addition of PGE2 resulted in actin filament depolymerization observable only in stretched cells. Our results indicate that key components of the eicosanoid pathway are upregulated by mechanically stimulated p38 MAP kinase in podocytes. Enhanced EP4 receptor signaling may undermine podocyte cytoskeletal dynamics and thereby compromise filtration barrier function under conditions of increased Pgc.


2005 ◽  
Vol 37 (3) ◽  
pp. 186-192 ◽  
Author(s):  
Jae-We Cho ◽  
Kun Park ◽  
Gi Ryang Kweon ◽  
Byeong-Churl Jang ◽  
Won-Ki Baek ◽  
...  

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