Effects of Melatonin on Blood Pressure, Oxidative Stress and Placental Expressions of TNFα, IL-6, VEGF and sFlt-1 in RUPP Rat Model of Preeclampsia

Oxidative stress is an imbalance between free radicals and antioxidants, and is an important etiological factor in the development of hypertension. Recent experimental evidence suggests that subpressor doses of angiotensin II elevate oxidative stress and blood pressure. We aimed to investigate the oxidative stress related mechanism by which a subpressor dose of angiotensin II induces hypertension in a normotensive rat model. Normotensive male Wistar rats were infused with a subpressor dose of angiotensin II for 28 days. The control group was sham operated and infused with saline only. Plasma angiotensin II and H2O2 levels, whole-blood glutathione peroxidase, and AT-1a, Cu/Zn SOD, and p22phox mRNA expression in the aorta was assessed. Systolic and diastolic blood pressures were elevated in the experimental group. There was no change in angiotensin II levels, but a significant increase in AT-1a mRNA expression was found in the experimental group. mRNA expression of p22phox was increased significantly and Cu/Zn SOD decreased significantly in the experimental group. There was no significant change to the H2O2 and GPx levels. Angiotensin II manipulates the free radical-antioxidant balance in the vasculature by selectively increasing O2− production and decreasing SOD activity and causes an oxidative stress induced elevation in blood pressure in the Wistar rat.

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Homeopathic Medicine Rauwolfia Serpentina Ameliorate Blood Pressure and Oxidative Stress Parameters of Kidney by Modulating Expression of Antioxidant Enzymes in Deoxycorticosterone Acetate (DOCA)-Salt-Induced Hypertensive Rat Model

Journal of Drug Research and Development ◽

10.16966/2470-1009.111 ◽

2016 ◽

Vol 2 (1) ◽

Cited By ~ 1

Author(s):

Kumar S

Keyword(s):

Oxidative Stress ◽

Blood Pressure ◽

Antioxidant Enzymes ◽

Rat Model ◽

Deoxycorticosterone Acetate ◽

Oxidative Stress Parameters ◽

Rauwolfia Serpentina ◽

Homeopathic Medicine ◽

And Oxidative Stress ◽

Stress Parameters

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Protective Effects of Pterostilbene Against Cardiac Oxidative Stressand Dysfunctionin Nicotine-Induced Cardiac Injury Rat Model

Biomedical & Pharmacology Journal ◽

10.13005/bpj/2164 ◽

2021 ◽

Vol 14 (02) ◽

pp. 623-633

Author(s):

Ahmad Rohi Ghazali ◽

Elancheleyen Mahindran ◽

Anand Ramalingam ◽

Liya Chee ◽

Satirah Zainalabidin

Keyword(s):

Oxidative Stress ◽

Blood Pressure ◽

Rat Model ◽

Systolic Dysfunction ◽

Cardiac Injury ◽

Left Ventricular ◽

Study Endpoint ◽

Tbars Level ◽

Protective Effects ◽

Sprague Dawley

Prolonged nicotine exposureescalates the onset and development of cardiovascular diseasesin both active and passive smokers via cardiac injury. Pterostilbene, a resveratrol derivative, has been shown to exhibit high anti-inflammatory,antioxidant and antitumor properties. Nevertheless, its role as a cardioprotective agent in a nicotine-induced rat model is still scarce. Therefore, our study was aimed to investigatethe effects of co-administered pterostilbene against nicotine-induced cardiac injury rat model.Twenty-six male Sprague-Dawley rats were randomly allotted and treated with nicotine (0.6 mg/kg)orin-combination with pterostilbene (10 mg/kg) for 28 consecutive days. Non-invasive tail cuff blood pressure measurements were taken atday-0, day-14 and day-28. Rat hearts were harvested at study endpoint and thechanges in cardiac function parameters and oxidative stress markers were evaluated. The findings have shown that pterostilbene co-administration significantly (P<0.05) reduced the blood pressure and ameliorated nicotine-induced cardiac systolic dysfunction by improving the left ventricular developed pressure (LVDP). In addition, pterostilbene also significantly (P <0.05)attenuatedthe thiobarbituric acid reactive substances (TBARS) level, indicative of protection against nicotine-induced cardiac oxidative stress. In summary, our findings suggest that pterostilbene has the potential to be developed as a natural alternative in protecting the cardiac injuryinduced by nicotine. However further studies are warranted to investigate its efficacy and the underlying mechanism in cardioprotection.

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Effect of sodium tanshinone IIA sulfonate treatment in a rat model of preeclampsia

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00222.2014 ◽

2015 ◽

Vol 308 (3) ◽

pp. R163-R172 ◽

Cited By ~ 10

Author(s):

Jude S. Morton ◽

Anita Quon ◽

Po-Yin Cheung ◽

Tatsuya Sawamura ◽

Sandra T. Davidge

Keyword(s):

Oxidative Stress ◽

Blood Pressure ◽

Rat Model ◽

Salvia Miltiorrhiza ◽

Oxidized Ldl ◽

Maternal Blood ◽

Tanshinone Iia ◽

Sodium Tanshinone Iia Sulfonate ◽

Paf Receptor ◽

Maternal Blood Pressure

Preeclampsia is a disorder of pregnancy with a significant impact on maternal and fetal health. The complexity of this multifactorial condition has precluded development of effective therapies and, although many potential pathways have been investigated, the etiology still requires clarification. Our group has investigated the scavenger lectin-like oxidized LDL (LOX-1) receptor, which may respond to factors released from the distressed placenta that contribute to the vascular pathologies observed in preeclampsia. Given the known beneficial effects of sodium tanshinone IIA sulfonate (STS; a component of Salvia miltiorrhiza) on vasodilation, reduction of oxidative stress, and lipid profiles, we have investigated its role as a potential treatment strategy. We hypothesized that STS would improve vascular endothelial function and, combined with a reduction in oxidative stress, would improve pregnancy outcomes in a rat model of preeclampsia (reduced uteroplacental perfusion pressure, RUPP). We further hypothesized this may occur via the action of STS on the LOX-1 and/or platelet-activating factor (PAF) receptor axes. The RUPP model increased maternal blood pressure, vascular oxidative stress, and involvement of the vascular PAF receptor. Treatment with STS during pregnancy decreased both oxidative stress and involvement of the PAF receptor; however, it also increased involvement of the LOX-1 receptor, which is in line with the concept that scavenger receptors, such as LOX-1 and PAF, are upregulated in response to ligand binding and/or under pathological conditions. In this model of preeclampsia, however, the vascular actions of STS did not lead to improvements in pregnancy outcome such as fetal biometrics or maternal blood pressure.

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Melatonin attenuates hypertension and oxidative stress in a rat model of L-NAME-induced gestational hypertension

Vascular Medicine ◽

10.1177/1358863x20919798 ◽

2020 ◽

Vol 25 (4) ◽

pp. 295-301 ◽

Cited By ~ 1

Author(s):

Junfang Zuo ◽

Ziyun Jiang

Keyword(s):

Oxidative Stress ◽

Blood Pressure ◽

Protein Content ◽

Rat Model ◽

Gestational Hypertension ◽

Systemic Disease ◽

Fetal Weight ◽

Therapeutic Effects ◽

Urine Protein ◽

Plasma Antioxidant Capacity

Preeclampsia is a life-threatening multiorgan systemic disease with manifestations including gestational hypertension, oxidative stress, and vascular dysfunction. We aimed to evaluate the therapeutic effects of melatonin on an L-NAME (NLG-nitro-l-arginine methyl ester)-induced rat preeclampsia model. During gestation, L-NAME was added to drinking water at 50 mg/kg/day from gestation day (GD) 8. Rats received the combination of L-NAME with melatonin (10 mg/kg/day), or aspirin (1.5 mg/kg/day), and rats that received only L-NAME or no treatments were used as controls. Aspirin was mixed with rodent chow and melatonin was administered intraperitoneally. Blood pressure and urine protein content were monitored every 3 days. On GD19, blood samples were collected for biochemical analysis. Compared to untreated L-NAME rats, melatonin led to markedly lowered blood pressure and urine protein content, and recovery in the fetus alive ratio, fetal weight, and the fetal weight/placental weight ratio. Compared to untreated L-NAME rats, plasma antioxidant capacity and plasma malondialdehyde were increased and decreased by melatonin, respectively, in L-NAME rats. Melatonin treatment also reduced sFlt-1, increased PlGF, and decreased the sFlt-1/PlGF ratio. In the placenta, melatonin also reduced sFlt-1 levels and increased Nrf2, PlGF, and HO-1 levels. We have demonstrated in a rat model of preeclampsia that melatonin exerts significant protective effects through lowering blood pressure and reducing oxidative stress.

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Faculty Opinions recommendation of High-intensity interval training beneficial effects on body mass, blood pressure, and oxidative stress in diet-induced obesity in ovariectomized mice.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.726692682.793522525 ◽

2016 ◽

Author(s):

Jerome Fleg

Keyword(s):

Oxidative Stress ◽

Blood Pressure ◽

High Intensity ◽

Interval Training ◽

High Intensity Interval Training ◽

Beneficial Effects ◽

Diet Induced Obesity ◽

Ovariectomized Mice ◽

High Intensity Interval ◽

And Oxidative Stress

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Protective Effect of Swertiamarin on Myocardial Injury Through Activation of Nrf2/HO-1 Pathway in Heart Failure Model of Rats

Current Topics in Nutraceutical Research ◽

10.37290/ctnr2641-452x.18:260-265 ◽

2020 ◽

Vol 18 (3) ◽

pp. 260-265

Author(s):

Xu Lin ◽

Zheng Xiaojun ◽

Lv Heng ◽

Mo Yipeng ◽

Tong Hong

Keyword(s):

Oxidative Stress ◽

Heart Failure ◽

Ejection Fraction ◽

Protective Effect ◽

Infarct Size ◽

Rat Model ◽

Left Ventricular ◽

Related Factor ◽

Nuclear Factor ◽

Internal Dimension

The purpose of this study was to evaluate the protective effect of swertiamarin on heart failure. To this end, a rat model of heart failure was established via left coronary artery ligation. Infarct size of heart tissues was determined using triphenyl tetrazolium chloride staining. Echocardiography was performed to evaluate cardiac function by the determination of ejection fraction, left ventricular internal dimension in diastole and left ventricular internal dimension in systole. The effect of swertiamarin on oxidative stress was evaluated via enzyme-linked immunosorbent assay. The mechanism was evaluated using western blot. Administration of swertiamarin reduced the infarct size of heart tissues in rat models with heart failure. Moreover, swertiamarin treatment ameliorated the cardiac function, increased ejection fraction and fractional shortening, decreased left ventricular internal dimension in diastole and left ventricular internal dimension in systole. Swertiamarin improved oxidative stress with reduced malondialdehyde, while increased superoxide dismutase, glutathione, and GSH peroxidase. Furthermore, nuclear-factor erythroid 2-related factor 2, heme oxygenase and NAD(P)H dehydrogenase (quinone 1) were elevated by swertiamarin treatment in heart tissues of rat model with heart failure. Swertiamarin alleviated heart failure through suppression of oxidative stress response via nuclear-factor erythroid 2-related factor 2/heme oxygenase-1 pathway providing a novel therapeutic strategy for heart failure.

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