Combined Effect of Estrogen Replacement and Angiotensin II Type I Receptor Blocker on Endothelial Dysfunction and Oxidative Stress in Ovariectomized Rats

2013 ◽  
Vol 42 (4) ◽  
pp. 553-568
Author(s):  
Sohair A. Saleh ◽  
Mamdouh R. El-Ridi ◽  
Suzan M. Hazza
Keyword(s):  
Oxidative Stress ◽  
Angiotensin Ii ◽  
Endothelial Dysfunction ◽  
Combined Effect ◽  
Receptor Blocker ◽  
Ovariectomized Rats ◽  
Type I ◽  
Estrogen Replacement ◽  
And Oxidative Stress

scholarly journals Resveratrol Supplementation Protects Against Nicotine-Induced Kidney Injury

2019 ◽  
Vol 16 (22) ◽  
pp. 4445 ◽  
Author(s):  
Ramalingam ◽  
Santhanathas ◽  
Shaukat Ali ◽  
Zainalabidin
Keyword(s):  
Oxidative Stress ◽  
Angiotensin Ii ◽  
Prolonged Exposure ◽  
Kidney Injury ◽  
Receptor Blocker ◽  
Renal Diseases ◽  
Angiotensin Ii Receptor Blocker ◽  
Type I ◽  
Sprague Dawley ◽  
And Oxidative Stress

Prolonged exposure to nicotine accelerates onset and progression of renal diseases in habitual cigarette smokers. Exposure to nicotine, either via active or passive smoking is strongly shown to enhance renal oxidative stress and augment kidney failure in various animal models. In this study, we investigated the effects of resveratrol supplementation on nicotine-induced kidney injury and oxidative stress in a rat model. Male Sprague-Dawley rats were given nicotine (0.6 mg/kg, i.p.) alone or in combination with either resveratrol (8 mg/kg, i.p.), or angiotensin II type I receptor blocker, irbesartan (10 mg/kg, p.o.) for 28 days. Upon completion of treatment, kidneys were investigated for changes in structure, kidney injury markers and oxidative stress. Administration of nicotine alone for 28 days resulted in significant renal impairment as shown by marked increase in plasma creatinine, blood urea nitrogen (BUN) and oxidative stress. Co-administration with resveratrol however successfully attenuated these changes, with a concomitant increase in renal antioxidants such as glutathione similar to the conventionally used angiotensin II receptor blocker, irbesartan. These data altogether suggest that targeting renal oxidative stress with resveratrol could alleviate nicotine-induced renal injury. Antioxidants may be clinically important for management of renal function in habitual smokers.

Abstract 1476: Angiotensin II Induced Hypertrophic Response And Oxidative Stress Is Attenuated In Mice Lacking The Gene For Tnf-α

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Srinivas Sriramula ◽  
Nithya Mariappan ◽  
Elizabeth McILwain ◽  
Joseph Francis
Keyword(s):  
Oxidative Stress ◽  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Collagen Type ◽  
Resonance Spectroscopy ◽  
Type I ◽  
Ang Ii ◽  
Hypertrophic Response ◽  
Tnf Α ◽  
And Oxidative Stress

Tumor necrosis factor-alpha (TNF-α) and angiotensin II (Ang II) play an important role in the pathophysiology of cardiovascular disease in part by inducing the cardiac hypertrophic response and oxidative stress. Recently we demonstrated that angiotensin induced hypertensive response is attenuated in mice lacking the gene for TNF-α. In this study, we examined whether Ang II induced cardiac hypertrophy and increased oxidative stress is mediated through TNF-α. Methods and results: Male TNF-α (−/−) and age matched control (WT) mice were subcutaneously implanted with osmotic minipumps containing Ang II (1 μg/kg/min) or saline for 14 days. Human recombinant TNF-α was injected in one group of TNF-α (−/−) mice (10 μg/kg/day) for 14 days. In WT+Ang mice, a temporal increase in blood pressure was observed during the study as measured by radio telemetry transmitters. At the end of the study, echocardiography revealed an increase in thickness and dimensions of left ventricle (LV) and decreased fractional shortening (%FS) in WT+Ang mice. Real time RT-PCR showed that Ang II- infusion resulted in an increase in heart/bodyweight ratio and of cardiac hypertrophy markers ANP and BNP, and profibrotic genes Collagen Type I, Collagen Type II, and TGF-β in WT mice. Electron Spin resonance spectroscopy revealed an increase in total ROS, superoxide and peroxynitrite in the WT+ANG mice when compared to control WT mice. However, these changes were all attenuated in TNF-α (−/−)+Ang mice. Ang II infusion also increased significantly the mRNA expression of gp91Phox, NOX-1, NOX-4 and AT1R in the LV of WT mice, but not in TNF-α (−/−) mice. Interestingly, injection of TNF-α in the TNF-α (−/−) mice, treated with Ang II resulted in increased cardiac hypertrophy and oxidative stress. Conclusions: Findings from the present study suggest that TNF-α plays an important role in the development of cardiac hypertrophy and oxidative stress in Ang II-induced hypertension.

scholarly journals Comparative effects of estrogen, raloxifene and tamoxifen on endothelial dysfunction, inflammatory markers and oxidative stress in ovariectomized rats

Life Sciences ◽  
2015 ◽  
Vol 124 ◽  
pp. 101-109 ◽  
Author(s):  
Aline Zandonadi Lamas ◽  
Izabela Facco Caliman ◽  
Polyana Lima Meireles Dalpiaz ◽  
Antônio Ferreira de Melo ◽  
Glaucia Rodrigues Abreu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Inflammatory Markers ◽  
Ovariectomized Rats ◽  
And Oxidative Stress

Combination treatment of angiotensin II type I receptor blocker and new oral iron chelator attenuates progression of nonalcoholic steatohepatitis in rats

2011 ◽  
Vol 300 (6) ◽  
pp. G1094-G1104 ◽  
Author(s):  
Kosuke Kaji ◽  
Hitoshi Yoshiji ◽  
Mitsuteru Kitade ◽  
Yasuhide Ikenaka ◽  
Ryuichi Noguchi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Amino Acid ◽  
Angiotensin Ii ◽  
Liver Fibrosis ◽  
Combination Treatment ◽  
Iron Chelator ◽  
Receptor Blocker ◽  
Type I ◽  
Oral Iron Chelator

Angiotensin II type I receptor blocker and iron chelator reportedly exert suppressive effects on nonalcoholic steatohepatitis (NASH) progression, including liver fibrosis and hepatocarcinogenesis. The aim of this study was to elucidate the combined effect of losartan (LOS), an angiotensin II type I receptor blocker, and deferasirox (DSX), a newly developed oral iron chelator, on the progression of NASH in rats. To induce NASH, F344 rats were fed a choline-deficient l-amino acid-defined diet for 12 wk, and the effects of LOS and DSX at clinically comparable low doses were elucidated in conjunction with oxidative stress, neovascularization, and hepatic stellate cells (HSC) activation, all known to play important roles in the progression of NASH. Treatment with both LOS and DSX suppressed choline-deficient l-amino acid-defined diet-induced liver fibrosis development and hepatocarcinogenesis. This combination treatment exerted a stronger inhibitory effect compared with treatment with a single agent. These inhibitory effects occurred almost concurrently with the suppression of oxidative stress, neovascularization, and HSC activation. Our in vitro study demonstrated that LOS and DSX inhibited angiotensin II-induced proliferation, transforming growth factor-β1 expression of activated HSC, and in vitro angiogenesis. These results indicated that dual inhibition by combined treatment of LOS and DSX attenuated the progression of NASH. Since both agents are widely used in clinical practice, this combination therapy may represent a potential new strategy against NASH in the near future.

Abstract 412: The Sodium-Glucose Cotransporter 2 Inhibitor Empagliflozin Improves Diabetic Complications in the Streptozotocin Type 1 Diabetes Mellitus Model by Interfering With Glucotoxicity and Rescue of Beta-Cell Function

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Philipp Welschof ◽  
Matthias Oelze ◽  
Swenja Kröller-Schön ◽  
Thomas Jansen ◽  
Michael Hausding ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Type I Diabetes ◽  
Cardiovascular Complications ◽  
Diabetic Rats ◽  
Low Grade ◽  
Type I ◽  
Urinary Glucose ◽  
And Oxidative Stress

Objectives: In diabetes, cardiovascular complications are associated with endothelial dysfunction and oxidative stress. Empagliflozin (Empa), as a selective sodium-glucose co-transporter 2 inhibitor (SGLT2i) in clinical development, offers a promising novel approach for the treatment of type 2 diabetes by enhancing urinary glucose excretion. The aim of the present study was to test whether treatment with Empa could improve endothelial dysfunction in type I diabetic rats via reduction of glucotoxicity and associated oxidative stress. Research Design and Methods: Type I diabetes in Wistar rats was induced by an intravenous injection of streptozotocin (60 mg/kg). One week after injection Empa was administered via drinking water for 7 weeks. Results: Treatment with Empa (10 and 30 mg/kg/d), showed reduction of blood glucose and a normalization of endothelial dysfunction (aortic rings) in diabetic rats and a reduced oxidative stress in aortic vessels (dihydroethidine staining) and in blood (phorbol ester/zymosan A-stimulated chemiluminescence). Additionally, the pro-inflammatory phenotype and glucotoxicity in diabetic animals was normalized by SGLT2i therapy. Conclusion: In this study we could demonstrate that Empa improves hyperglycemia and prevents the development of endothelial dysfunction and oxidative stress in type 1 diabetic rats. Future studies will investigate the underlying mechanisms of these antioxidant and anti-inflammatory effects with special emphasis on low-grade inflammation, glucotoxicity and oxidative stress, all of which contributes to cardiovascular complications.

Estrogen Replacement Suppresses Pressor Response and Oxidative Stress Induced by Cage-switch Stress in Ovariectomized Rats

2008 ◽  
Vol 1148 (1) ◽  
pp. 213-218 ◽  
Author(s):  
Keiko Morimoto ◽  
Masami Uji ◽  
Takashi Ueyama ◽  
Hiroko Kimura ◽  
Tomomi Kohno ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pressor Response ◽  
Ovariectomized Rats ◽  
Estrogen Replacement ◽  
And Oxidative Stress
Sign in / Sign up

Export Citation Format

Share Document