Ganglioside GD1a Suppression of NOS2 Expression Via ERK1 Pathway in Mouse Osteosarcoma FBJ Cells

2010 ◽  
Vol 110 (5) ◽  
pp. 1165-1174 ◽  
Author(s):  
Ting Cao ◽  
Tianyi Zhang ◽  
Li Wang ◽  
Lan Zhang ◽  
Tomoko Adachi ◽  
...  
2001 ◽  
Vol 94 (3) ◽  
pp. 328-334 ◽  
Author(s):  
Sumiko Hyuga ◽  
Nana Kawasaki ◽  
Masashi Hyuga ◽  
Miyako Ohta ◽  
Rie Shibayama ◽  
...  

Author(s):  
Alexander T Sougiannis ◽  
Brandon N. VanderVeen ◽  
Ioulia Chatzistamou ◽  
Jason L Kubinak ◽  
Mitzi Nagarkatti ◽  
...  

Emodin, a natural anthraquinone, has been shown to have anti-tumorigenic properties and may be an effective therapy for colorectal cancer (CRC). However, its clinical development has been hampered by a poor understanding of its mechanism of action. The purpose of this study was to 1) evaluate the efficacy of emodin in mouse models of intestinal/colorectal cancer and 2) to examine the impact of emodin on macrophage behavior in the context of CRC. We utilized a genetic model of intestinal cancer (ApcMin/+) and a chemically induced model of CRC (AOM/DSS). Emodin was administered orally (40 mg/kg or 80 mg/kg in AOM/DSS and 80mg/kg in ApcMin/+) 3x/week to observe its preventative effects. Emodin reduced polyp count and size in both rodent models (p<0.05). We further analyzed the colon microenvironment of AOM/DSS mice and found that mice treated with emodin exhibited lower pro-tumorigenic M2-like macrophages and a reduced ratio of M2/M1 macrophages within the colon (p<0.05). Despite this, we did not detect any significant changes in M2-associated cytokines (IL10, IL4, and Tgfb1) nor M1-associated cytokines (IL6, TNFα, IL1β, and IFNγ) within excised polyps. However, there was a significant increase in NOS2 expression (M1 marker) in mice treated with 80 mg/kg emodin (p<0.05). To confirm emodin's effects on macrophages, we exposed bone marrow-derived macrophages (BMDMs) to C26 colon cancer cell conditioned media. Supporting our in vivo data, emodin reduced M2-like macrophages. Overall, these data support the development of emodin as a natural compound for prevention of CRC given its ability to target pro-tumor macrophages.


2020 ◽  
Vol 44 (2) ◽  
pp. 83-88
Author(s):  
Malena Boylan ◽  
Megan B. O’Brien ◽  
Charlotte Beynon ◽  
Kieran G. Meade

1977 ◽  
Vol 78 (2) ◽  
pp. 333-339 ◽  
Author(s):  
J. Schraven ◽  
C. Čáp ◽  
G. Nowoczek ◽  
K. Sandhoff

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 887
Author(s):  
Sergio Rius-Pérez ◽  
Isabel Torres-Cuevas ◽  
María Monsalve ◽  
Francisco J. Miranda ◽  
Salvador Pérez

Acute pancreatitis is an inflammatory process of the pancreatic tissue that often leads to distant organ dysfunction. Although liver injury is uncommon in acute pancreatitis, obesity is a risk factor for the development of hepatic complications. The aim of this work was to evaluate the role of PGC-1α in inflammatory response regulation in the liver and its contribution to the detrimental effect of obesity on the liver during acute pancreatitis. For this purpose, we induced acute pancreatitis by cerulein in not only wild-type (WT) and PGC-1α knockout (KO) mice, but also in lean and obese mice. PGC-1α levels were up-regulated in the mice livers with pancreatitis. The increased PGC-1α levels were bound to p65 to restrain its transcriptional activity toward Nos2. Lack of PGC-1α favored the assembly of the p65/phospho-STAT3 complex, which promoted Nos2 expression during acute pancreatitis. The increased transcript Nos2 levels and the pro-oxidant liver status caused by the down-regulated expression of the PGC-1α-dependent antioxidant genes enhanced nitrosative stress and decreased energy charge in the livers of the PGC-1α KO mice with pancreatitis. It is noteworthy that the PGC-1α levels lowered in the obese mice livers, which increased the Nos2 mRNA expression and protein nitration levels and decreased energy charge during pancreatitis. In conclusion, obesity impairs PGC-1α up-regulation in the liver to cause nitrosative stress during acute pancreatitis.


1999 ◽  
Vol 5 (6) ◽  
pp. 379-388 ◽  
Author(s):  
S. Matà ◽  
F. Lolli ◽  
M. Söderström ◽  
F. Pinto ◽  
H. Link

2004 ◽  
Vol 32 (Supplement) ◽  
pp. A129
Author(s):  
Derek S Wheeler ◽  
Hector R Wong ◽  
Paul Hake ◽  
Basilia Zingarelli ◽  
Connie Snead ◽  
...  

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