Anti-atherosclerotic effect of housefly (Musca domestica) maggot-derived protein-enriched extracts by dampened oxidative stress in apolipoprotein E-deficient mice

RSC Advances ◽  
2016 ◽  
Vol 6 (107) ◽  
pp. 105363-105370 ◽  
Author(s):  
Xiao Mingzhu ◽  
Jin Xiaobao ◽  
Tang Futian ◽  
Wang Lijing ◽  
Mao Jianwen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Apolipoprotein E ◽  
Musca Domestica ◽  
Developed Countries ◽  
Morbidity And Mortality ◽  
Deficient Mice

Despitemany therapeutic advances, atherosclerosis remains the leading cause of morbidity and mortality in developed countries.

scholarly journals Absence of 12/15 Lipoxygenase Reduces Brain Oxidative Stress in Apolipoprotein E-Deficient Mice

2005 ◽  
Vol 167 (5) ◽  
pp. 1371-1377 ◽  
Author(s):  
Cinzia M. Chinnici ◽  
Yuemang Yao ◽  
Tao Ding ◽  
Colin D. Funk ◽  
Domenico Praticò
Keyword(s):  
Oxidative Stress ◽  
Apolipoprotein E ◽  
Brain Oxidative Stress ◽  
Deficient Mice

scholarly journals Chronic iron overload intensifies atherosclerosis in apolipoprotein E deficient mice: Role of oxidative stress and endothelial dysfunction

Life Sciences ◽  
2019 ◽  
Vol 233 ◽  
pp. 116702 ◽  
Author(s):  
Vinícius Bermond Marques ◽  
Marcos André Soares Leal ◽  
Jandinay Gonzaga Alexandre Mageski ◽  
Helbert Gabriel Fidelis ◽  
Breno Valentim Nogueira ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Iron Overload ◽  
Apolipoprotein E ◽  
Deficient Mice

Dietary restriction reduces atherosclerosis and oxidative stress in the aorta of apolipoprotein E-deficient mice

2002 ◽  
Vol 123 (8) ◽  
pp. 1121-1131 ◽  
Author(s):  
ZhongMao Guo ◽  
Felicia Mitchell-Raymundo ◽  
Hong Yang ◽  
Yuji Ikeno ◽  
James Nelson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Apolipoprotein E ◽  
Dietary Restriction ◽  
And Oxidative Stress ◽  
Deficient Mice

Abstract 461: Cilnidipine Attenuated Angiotensin II-induced Abdominal Aortic Aneurysms in Apolipoprotein E-deficient Mice

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Yuki Kakio ◽  
Haruhito A Uchida ◽  
Ryoko Umebayashi ◽  
Jun Wada
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Angiotensin Ii ◽  
Apolipoprotein E ◽  
Ex Vivo ◽  
Abdominal Aortic Aneurysms ◽  
Aortic Aneurysms ◽  
Osmotic Minipumps ◽  
Abdominal Aortic ◽  
Deficient Mice

Objective: Chronic infusion of angiotensin II (AngII) promotes development of abdominal aortic aneurysms (AAAs) in hypercholesterolemic mice. Previous studies have shown that local inflammation and increased oxidative stress plays an important role on formation of AAAs. In addition, it is reported that voltage-dependent N-type Ca2+ channels in endothelial cells contribute to oxidative stress-related endothelial dysfunction induced by AngII in mice. Therefore, we hypothesized that cilnidipine, an N/L-type calcium channel blocker, exerts vasoprotective effect by inhibiting inflammation and superoxide generation in mice. The purpose of this study was to evaluate whether cilnidipine influenced AngII-induced AAAs. Methods and Results: Male apolipoprotein E deficient mice (8-12 weeks old) were fed a normal laboratory diet. Mice were infused subcutaneously with either cilnidipine or vehicle by osmotic minipumps. Three days later, mice were also infused subcutaneously with either AngII (1,000 ng/kg/min, n = 14-16) or saline (n = 4) each by osmotic minipumps for 4 weeks. AngII increased systolic blood pressure. Cilnidipine decreased blood pressure in AngII-infused mice, but had not effect during saline infusion. AngII infusion did not alter serum cholesterol concentrations. However, cilnidipine slightly decreased serumcholesterol concentrations in AngII-infused mice. Cilnidipine had no effect on body weights, heart rates, and urine total protein, but mildly restored plasma renin activity that were suppressed by AngII infusion. Cilnidipine did not affect ex vivo measurement of maximal diameter of abdominal aorta (1.04 ± 0.09 mm vs 1.11 ± 0.06 mm, n.s.) in saline infused mice. AngII infusion significantly increased ex vivo maximal diameters of abdominal aortas, but was attenuated by cilnidipine (1.79 ± 0.59 mm vs 1.26 ± 0.38 mm, P < 0.05). In addition, cilnidipine significantly reduced the incidence of AngII-induced AAAs (Cilnidipine: 38 %, Vehicle: 88 %; P < 0.05). Furthermore, gelatin zymography demonstrated that cilnidipine diminished AngII-induced increase in aortic MMP-9 protein abundance. Conclusion: Cilnidipine attenuated AngII-induced AAAs in male apolipoprotein E deficient mice.

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