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| 1 | Inflammation, oxidative stress and renin angiotensin system in atherosclerosis显示文摘Atherosclerosis is a chronic inflammatory disease associated with cardiovascular dysfunction including myocardial infarction, unstable angina, sudden cardiac death, stroke and peripheral thromboses. It has been predicted that atherosclerosis will be the primary cause of death in the world by 2020. Atherogenesis is initiated by endothelial injury due to oxidative stress associated with cardiovascular risk factors including diabetes mellitus, hypertension, cigarette smoking, dyslipidemia, obesity, and metabolic syndrome. The impairment of the endothelium associated with cardiovascular risk factors creates an imbalance between vasodilating and vasoconstricting factors, in particular, an increase in angiotensin Ⅱ(Ang Ⅱ) and a decrease in nitric oxide. The renin-angiotensin system(RAS), and its primary mediator Ang Ⅱ, also have a direct influence on the progression of the atherosclerotic process via effects on endothelial function, inflammation, fibrinolytic balance, and plaque stability. Anti-inflammatory agents [statins, secretory phospholipase A2 inhibitor, lipoprotein-associated phospholipase A2 inhibitor, 5-lipoxygenase activating protein, chemokine motif ligand-2, C-C chemokine motif receptor 2 pathway inhibitors, methotrexate, IL-1 pathway inhibitor and RAS inhibitors(angiotensin-converting enzyme inhibitors)], Ang Ⅱ receptor blockers and ranin inhibitors may slow inflammatory processes and disease progression. Several studies in human using anti-inflammatory agents and RAS inhibitors revealed vascular benefits and reduced progression of coronary atherosclerosis in patients with stable angina pectoris; decreased vascular inflammatory markers, improved common carotid intima-media thickness and plaque volume in patients with diagnosed atherosclerosis. Recent preclinical studies have demonstrated therapeutic efficacy of vitamin D analogs paricalcitol in Apo E-deficient atherosclerotic mice. | Kazim Husain Wilfredo Hernandez Rais A Ansari Leon Ferder | 2015 | World Journal of Biological Chemistry2015，6，3： | 84 |
| 2 | Alcohol-induced hypertension: Mechanism and prevention显示文摘Epidemiological, preclinical and clinical studies es-tablished the association between high alcohol con-sumption and hypertension. However the mechanism through which alcohol raises blood pressure remains elusive. Several possible mechanisms have been pro-posed such as an imbalance of the central nervous system, impairment of the baroreceptors, enhanced sympathetic activity, stimulation of the renin-angio-tensin-aldosterone system, increased cortisol levels, increased vascular reactivity due to increase in intracel-lular calcium levels, stimulation of the endothelium to release vasoconstrictors and loss of relaxation due to inflammation and oxidative injury of the endothelium leading to inhibition of endothelium-dependent nitric oxide production. Loss of relaxation due to inflamma-tion and oxidative injury of the endothelium by angio-tensin II leading to inhibition of endothelium-dependent nitric oxide production is the major contributors of the alcohol-induced hypertension. For the prevention of alcohol-induced hypertension is to reduce the amount of alcohol intake. Physical conditioning/exercise trainingis one of the most important strategies to prevent/treat chronic alcohol-induced hypertension on physiological basis. The efficacious pharmacologic treatment includes the angiotensin-converting enzyme(ACE) inhibitors or angiotensin Ⅱ type 1 receptor blockers(ARBs) which have antioxidant activity and calcium channel blockers. The most effective prevention and treatment of alcohol-induced hypertension is physical exercise and the use of ACE inhibitors or ARBs in the | Kazim Husain Rais A Ansari Leon Ferder | 2014 | World Journal of Cardiology2014，6，5： | 8 |
| 3 | Effects of Paricalcitol and Enalapril on Atherosclerotic Injury in Mouse Aortas显示文摘 | Husain Kazim Suarez Edu Isidro Angel Ferder Leon | 2010 | American Journal of Nephrology2010，，4： | 2 |
| 4 | Combination Therapy with Paricalcitol and Enalapril Ameliorates Cardiac Oxidative Injury in Uremic Rats显示文摘 | Husain Kazim Ferder Leon Mizobuchi Masahide Finch Jane Slatopolsky Eduardo | 2009 | American Journal of Nephrology2009，，5： | 2 |
| 5 | Chronic ethanol ingestion induces aortic inflammation/oxidative endothelial injury and hypertension in rats显示文摘 | Husain Kazim Ferder Leon Ansari Rais A Lalla Jainarine | 2011 | Human and Experimental Toxicology2011，，8： | 1 |
| 6 | Effect of paricalcitol and enalapril on renal inflammation/oxidative stress in atherosclerosis显示文摘AIM: To investigate the protective effect of paricalcitol and enalapril on renal inflammation and oxidative stress in Apo E-knock out mice. METHODS: Animals treated for 4 mo as group(1) Apo E-knock out plus vehicle, group(2) Apo E-knock out plus paricalcitol(200 ng thrice a week),(3) Apo Eknock out plus enalapril(30 mg/L),(4) Apo E-knock out plus paricalcitol plus enalapril and(5) normal. Blood pressure(BP) was recorded using tail cuff method. The kidneys were isolated for biochemical assays using spectrophotometer and Western blot analyses. RESULTS: Apo E-deficient mice developed high BP(127 ± 3 mm Hg) and it was ameliorated by enalapril and enalapril plus paricalcitol treatments but not with paricalcitol alone. Renal malondialdehyde concentrations, p22 phox, manganese-superoxide dismutase, inducible nitric oxide synthase(NOS), monocyte chemoattractant protein-1, tumor necrosis factor-alpha and transforming growth factor-β1 levels significantly elevated but reduced glutathione, Cu Zn-SOD and e NOS levels significantly depleted in Apo E-knock out animals compared to normal. Administration of paricalcitol, enalapril and combined together ameliorated the renal inflammation and oxidative stress in Apo E-knock out animals. CONCLUSION: Paricalcitol and enalapril combo treatment ameliorates renal inflammation as well as oxidative stress in atherosclerotic animals. | Kazim Husain Edu Suarez Angel Isidro Wilfredo Hernandez Leon Ferder | 2015 | World Journal of Biological Chemistry2015，6，3： | 1 |
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