scholarly journals Protection from hypertension in mice by the Mediterranean diet is mediated by nitro fatty acid inhibition of soluble epoxide hydrolase

2014 ◽  
Vol 111 (22) ◽  
pp. 8167-8172 ◽  
Author(s):  
R. L. Charles ◽  
O. Rudyk ◽  
O. Prysyazhna ◽  
A. Kamynina ◽  
J. Yang ◽  
...  
1973 ◽  
Vol 248 (6) ◽  
pp. 1901-1905
Author(s):  
Harry K. Delcher ◽  
George S. Eisenbarth ◽  
Harold E. Lebovitz

Nitric Oxide ◽  
2008 ◽  
Vol 19 ◽  
pp. 31
Author(s):  
Marsha P. Cole ◽  
Tanja Rudoph ◽  
Bruce A. Freeman ◽  
Philip Michael Bauer

ACS Omega ◽  
2018 ◽  
Vol 3 (10) ◽  
pp. 14076-14086 ◽  
Author(s):  
Sean D. Kodani ◽  
Debin Wan ◽  
Karen M. Wagner ◽  
Sung Hee Hwang ◽  
Christophe Morisseau ◽  
...  

2013 ◽  
Vol 33 (10) ◽  
pp. 868
Author(s):  
Alonso G.P. Guedes ◽  
David Hood ◽  
Jun-Yan Liu ◽  
Christophe Morisseau ◽  
Bruce Hammock

2018 ◽  
Vol 115 (20) ◽  
pp. 5283-5288 ◽  
Author(s):  
Weicang Wang ◽  
Jun Yang ◽  
Jianan Zhang ◽  
Yuxin Wang ◽  
Sung Hee Hwang ◽  
...  

Obesity is associated with enhanced colonic inflammation, which is a major risk factor for colorectal cancer. Considering the obesity epidemic in Western countries, it is important to identify novel therapeutic targets for obesity-induced colonic inflammation, to develop targeted strategies for prevention. Eicosanoids are endogenous lipid signaling molecules involved in regulating inflammation and immune responses. Using an LC-MS/MS–based lipidomics approach, we find that obesity-induced colonic inflammation is associated with increased expression of soluble epoxide hydrolase (sEH) and its eicosanoid metabolites, termed fatty acid diols, in colon tissue. Furthermore, we find that pharmacological inhibition or genetic ablation of sEH reduces colonic concentrations of fatty acid diols, attenuates obesity-induced colonic inflammation, and decreases obesity-induced activation of Wnt signaling in mice. Together, these results support that sEH could be a novel therapeutic target for obesity-induced colonic inflammation and associated diseases.


2020 ◽  
Vol 311 ◽  
pp. 123501 ◽  
Author(s):  
Weixin Zhao ◽  
Jinhui Jeanne Huang ◽  
Binbin Hua ◽  
Zhiyong Huang ◽  
Ronald L. Droste ◽  
...  

1990 ◽  
Vol 259 (4) ◽  
pp. H1079-H1085 ◽  
Author(s):  
J. J. McVeigh ◽  
G. D. Lopaschuk

We have previously shown that high concentrations of fatty acids depress reperfusion recovery of ischemic rat hearts as a result of a fatty acid inhibition of glucose oxidation. In this study, we determined whether dichloroacetate, an activator of pyruvate dehydrogenase, could overcome fatty acid inhibition of glucose oxidation and thereby improve mechanical recovery of hearts reperfused after a period of transient global ischemia. Isolated working rat hearts, perfused with 11 mM glucose, 1.2 mM palmitate, and 500 microU/ml insulin, were subjected to a 30-min period of no flow ischemia, followed by a 30-min period of reperfusion. Under these conditions, control hearts recovered 37% of preischemic function. The addition of 1 mM dichloroacetate to the perfusate at reperfusion resulted in a significant improvement in recovery of mechanical function (to 73% of preischemic function). When dichloroacetate was added before the onset of ischemia, however, this protective effect was lost, and a significant increase in myocardial lactate accumulation during ischemia was observed. The effects of dichloroacetate on glucose oxidation rates in both nonischemic and reperfused ischemic hearts was determined by perfusing hearts with 11 mM [U-14C]glucose and 1.2 mM palmitate and quantitatively collecting 14CO2 produced by the heart. In nonischemic hearts, 1 mM dichloroacetate increased steady-state glucose oxidation rates from 298 +/- 69 to 1,223 +/- 135 nmol.g dry wt-1.min-1. The addition of dichloroacetate to hearts reperfused after a 25-min period of ischemia also increased glucose oxidation rates from (112 +/- 25 to 561 +/- 83 nmol.g dry wt-1.min-1).(ABSTRACT TRUNCATED AT 250 WORDS)


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