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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 | Chronic ethanol and nicotine interaction on rat tissue antioxidant defense system显示文摘 | Kazim Husain Benjamin R. Scott Sathya K. Reddy Satu M. Somani | 2001 | Alcohol2001，，2： | 4 |
| 4 | Partial Protection by Lipoic Acid Against Carboplantin-induced Ototoxicity in Rats显示文摘Objective To investigate the alterations in auditory brainstem evoked responses (ABRs) and the changes of carboplatin-induced ototoxicity in the cochlear oxidant/antioxidant systems and otoprotection by an antioxidant lipoate. Methods Male wistar rats were divided into four groups and treated as follows: 1) vehicle (saline) control, 2) carboplatin (256 mg/kg, i.p.), 3) lipoate (100 mg/kg, i.p.), 4) lipoate + carboplatin. Post-treatment ABRs were performed after four days and rats were sacrificed with their cochleae harvested and analyzed. Results Carboplatin significantly elevated ABR threshold above the pretreatment thresholds. Lipoate+carboplatin treated rats showed decreased elevation of hearing threshold. Carboplatin significantly depleted cochlear reduced to oxizized glutathione (GSH/GSSG) ratio, whereas lipoate+carboplatin treatment increased GSH/GSSG ratio. Carboplatin significantly decreased cochlear copper zinc-superoxide dismutase (CuZn-SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR) and glutathione-S-transferase (GST) activities and enzyme protein expressions and a significant increase in Mn-SOD activity, protein expression and malondialdehyde (MDA) level. Cochlear antioxidant enzyme activities, enzyme protein expressions and MDA level were partially restored in lipoate+carboplatin treated rats, compared to carboplatin alone. Conclusion Carboplatin-induced ototoxicity is related to impairment of cochlear antioxidant system and otoprotection conferred by lipoate is associated with partial sparing of the cochlear antioxidant defense system. | KAZIM HUSAIN CRAIG WHITWORTH SATU M. SOMANI LEONARD P. RYBAK | 2005 | Biomedical and Environmental Sciences2005，18，3： | 3 |
| 5 | 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 |
| 6 | 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 |
| 7 | Chronic alcohol-induced oxidative endothelial injury relates to angiotensin II levels in the rat显示文摘 | Kazim Husain Manuel Vazquez Rais A. Ansari Mokenge P. Malafa Jainarine Lalla | 2008 | Molecular and Cellular Biochemistry (-)2008，，1： | 2 |
| 8 | Physiological basis for effect of physical conditioning on chronic ethanol-induced hypertension in a rat model显示文摘 | Kazim Husain Jose Mejia Jainarine Lalla | 2006 | Molecular and Cellular Biochemistry (-)2006，，1： | 2 |
| 9 | Chronic ethanol and nicotine interaction on rat tissue antioxidant defense system显示文摘 | Kazim Husain Benjamin R Scott Sathya K | 2001 | Alcohol2001，25，： | 1 |
| 10 | 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 |
| 11 | Plasma MicroRNAs as Novel Biomarkers for Patients with Intraductal Papillary Mucinous Neoplasms of the Pancreas显示文摘 | Jennifer Permuth-Wey Dung-Tsa Chen William J. Fulp Sean J. Yoder Yonghong Zhang Christina Georgeades Kazim Husain Barbara Ann Centeno Anthony M. Magliocco Domenico Coppola Mokenge Malafa | 2015 | Cancer Prevention Research2015，，9： | 1 |
| 12 | Allicin Attenuates Inflammation and Suppresses HLA-B27 Protein Expression in Ankylosing Spondylitis Mice显示文摘 | Xin Gu Haishan Wu Peiliang Fu Kazim Husain | 2013 | BioMed Research International2013，，： | 1 |
| 13 | Dose response of alcohol-induced changes in BP, nitric oxide and antioxidants in rat plasma显示文摘 | Kazim Husain Jose Mejia Jainarine Lalla Sheeba Kazim | 2004 | Pharmacological Research2004，，4： | 1 |
| 14 | Physical conditioning modulates rat cardiac vascular endothelial growth factor gene expression in nitric oxide-deficient hypertension显示文摘 | Kazim Husain | 2004 | Biochemical and Biophysical Research Communications2004，，4： | 1 |
| 15 | The Antidiabetic Effect of Low Doses of Moringa oleifera Lam. Seeds on Streptozotocin Induced Diabetes and Diabetic Nephropathy in Male Rats显示文摘 | Abdulrahman L. Al-Malki Haddad A. El Rabey Kazim Husain | 2015 | BioMed Research International2015，，： | 1 |
| 16 | Dose dependent protection by lipoic acid against cisplatin-induced ototoxicity in rats:antioxidant defense system显示文摘 | Leonard P Rybak Kazim Husain | 1999 | Toxicological Sciences1999，47，3： | 1 |
| 17 | Chronic alcohol-induced oxidative endothelial injury relates to angiotensin II levels in the rat显示文摘 | Kazim Husain Manuel Vazquez Rais A. Ansari Mokenge P. Malafa Jainarine Lalla | 2008 | Molecular and Cellular Biochemistry (-)2008，，1： | 1 |
| 18 | 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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