Perilla Oil Reduces Fatty Streak Formation at Aortic Sinus via Attenuation of Plasma Lipids and Regulation of Nitric Oxide Synthase in ApoE KO Mice

Lipids ◽  
2016 ◽  
Vol 51 (10) ◽  
pp. 1161-1170 ◽  
Author(s):  
Sun Hee Hong ◽  
Mijeong Kim ◽  
Jeong Sook Noh ◽  
Yeong Ok Song
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Plasma Lipids ◽  
Fatty Streak ◽  
Aortic Sinus ◽  
Perilla Oil ◽  
Apoe Ko Mice ◽  
Oxide Synthase ◽  
Apoe Ko

scholarly journals Insulin decreases atherosclerotic plaque burden and increases plaque stability via nitric oxide synthase in apolipoprotein E-null mice

2016 ◽  
Vol 311 (2) ◽  
pp. E335-E345 ◽  
Author(s):  
Yusaku Mori ◽  
Simon Chiang ◽  
Michelle P. Bendeck ◽  
Adria Giacca
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Apolipoprotein E ◽  
Atherosclerotic Plaque ◽  
Insulin Treatment ◽  
Plaque Burden ◽  
High Cholesterol Diet ◽  
Aortic Sinus ◽  
Plaque Stability ◽  
Oxide Synthase

It has been argued whether insulin accelerates or prevents atherosclerosis. Although results from in vitro studies have been conflicting, recent in vivo mice studies demonstrated antiatherogenic effects of insulin. Insulin is a known activator of endothelial nitric oxide synthase (NOS), leading to increased production of NO, which has potent antiatherogenic effects. We aimed to examine the role of NOS in the protective effects of insulin against atherosclerosis. Male apolipoprotein E-null mice (8 wk old) fed a high-cholesterol diet (1.25% cholesterol) were assigned to the following 12-wk treatments: control, insulin (0.05 U/day via subcutaneous pellet), Nω-nitro-l-arginine methyl ester hydrochloride (l-NAME, via drinking water at 100 mg/l), and insulin plus l-NAME. Insulin reduced atherosclerotic plaque burden in the descending aorta by 42% compared with control (plaque area/aorta lumen area: control, 16.5 ± 1.9%; insulin, 9.6 ± 1.3%, P < 0.05). Although insulin did not decrease plaque burden in the aortic sinus, macrophage accumulation in the plaque was decreased by insulin. Furthermore, insulin increased smooth muscle actin and collagen content and decreased plaque necrosis, consistent with increased plaque stability. In addition, insulin treatment increased plasma NO levels, decreased inducible NOS staining, and tended to increase phosphorylated vasodilator-stimulated phosphoprotein staining in the plaques of the aortic sinus. All these effects of insulin were abolished by coadministration of l-NAME, whereas l-NAME alone showed no effect. Insulin also tended to increase phosphorylated endothelial NOS and total neuronal NOS staining, effects not modified by l-NAME. In conclusion, we demonstrate that insulin treatment decreases atherosclerotic plaque burden and increases plaque stability through NOS-dependent mechanisms.

scholarly journals Paradoxical Reduction of Fatty Streak Formation in Mice Lacking Endothelial Nitric Oxide Synthase

Circulation ◽  
2002 ◽  
Vol 105 (17) ◽  
pp. 2078-2082 ◽  
Author(s):  
Weibin Shi ◽  
Xuping Wang ◽  
Diana M. Shih ◽  
Victor E. Laubach ◽  
Mohamad Navab ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Fatty Streak ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Localization of endothelial nitric oxide synthase in the normal and failing human atrial myocardium

1996 ◽  
Vol 54 ◽  
pp. 786-787
Author(s):  
Chi-Ming Wei ◽  
Margarita Bracamonte ◽  
Shi-Wen Jiang ◽  
Richard C. Daly ◽  
Christopher G.A. McGregor ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Cardiac Tissues ◽  
Mammalian Tissues ◽  
End Stage Heart Failure ◽  
End Stage ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).

Nitric oxide synthase and cellac disease

2001 ◽  
Vol 120 (5) ◽  
pp. A684-A684
Author(s):  
I DANIELS ◽  
I MURRAY ◽  
W GODDARD ◽  
R LONG
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Oxide Synthase

Inhibitory effect of melatonin on nitric oxide synthase in rat enteric nervous system

2001 ◽  
Vol 120 (5) ◽  
pp. A176-A176
Author(s):  
P KOPPITZ ◽  
M STORR ◽  
D SAUR ◽  
M KURJAK ◽  
H ALLESCHER
Keyword(s):  
Nitric Oxide ◽  
Nervous System ◽  
Nitric Oxide Synthase ◽  
Enteric Nervous System ◽  
Inhibitory Effect ◽  
Oxide Synthase

Nitric oxide synthase and cyclooxygenase expressions in different stages of human gastric adenocarcinoma

2001 ◽  
Vol 120 (5) ◽  
pp. A169-A169 ◽  
Author(s):  
A RAJNAKOVA ◽  
P GOH ◽  
S NGOI ◽  
S MOOCHHALA ◽  
S LIM
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Gastric Adenocarcinoma ◽  
Human Gastric Adenocarcinoma ◽  
Oxide Synthase
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