scholarly journals Beneficial effects of combined therapy with lacidipine and candesartan in obese hypertensive patients

2018 ◽  
Vol 56 (4) ◽  
pp. 257-264
Author(s):  
Tatiana Ashcheulova ◽  
Nina Gerasimchuk ◽  
Olga Kovalyova ◽  
Oleksii Honchar
Keyword(s):  
Oxidative Stress ◽  
Endothelial Function ◽  
Antihypertensive Therapy ◽  
Inflammatory Cytokines ◽  
Overweight And Obesity ◽  
Oxidative Stress Marker ◽  
Hypertensive Patients ◽  
Tnf Α ◽  
And Oxidative Stress ◽  
Pro Inflammatory Cytokines

Abstract Introduction. Obesity is becoming one of the leading risk factors of coronary heart disease, hypertension, cerebrovascular disease. Despite the presence of a large number of antihypertensive agents and scientific substantiation of antihypertensive treatment principles it would be wrong to assume that the problem is completely solved. Development of endothelial dysfunction is one of the key pathogenic mechanisms in hypertension. This process is proven to have contributed by immune inflammation activation which is mediated by pro-inflammatory cytokines and oxidative stress. Aims. To investigate the additional benefits of the combined antihypertensive therapy with lacidipine and candesartan on the basis of studying their antioxidant properties, impact on endothelial function and pro-inflammatory cytokines activity in hypertensive patients with overweight and obesity. Methods. A combination of a calcium channel blocker and angiotensin receptor blocker (lacidipine 2 mg, 4 mg, and candesartan 4mg, 8mg, 16mg) was prescribed to 30 patients with essential hypertension of grades 1-3, 30 to 65 years old (mean age - 54.7 ± 5.8 years), who previously have not been receiving regular antihypertensive therapy. Results. During the course of combined antihypertensive therapy with lacidipine and candesartan, a significant reduction in i-NOS activity, TNF-α to its type I soluble receptor ratio (TNF- α/sTNF-αRI), and oxidative stress marker - 8-iso-PgF2α has been observed. Activity of e-NOS, levels of SOD and catalase, in contrast, have increased by the end of observation period. Conclusion. The improvement of endothelial function due to lower level of oxidative stress and a significant decrease of immune activation has been observed in hypertensive patients with overweight and obesity under the influence of combined antihypertensive therapy with lacidipine and candesartan.

scholarly journals Peculiarities of the influence of antihypertensive therapy on endothelial function, oxidative stress and immune activation in obese patients

2017 ◽  
Vol 8 (2) ◽  
pp. 152-156 ◽  
Author(s):  
T. V. Ashcheulova ◽  
N. N. Gerasimchuk
Keyword(s):  
Oxidative Stress ◽  
Endothelial Function ◽  
Antihypertensive Therapy ◽  
Overweight And Obesity ◽  
Oxidative Stress Marker ◽  
Control Group ◽  
Type I ◽  
Soluble Receptor ◽  
Hypertensive Patients ◽  
Tnf Α

This article aims to improve combined antihypertensive therapy on the basis of studying the antioxidant properties of bisoprolol and indapamid, their impact on endothelial dysfunction (ED) and pro-inflammatory cytokines activity in hypertensive patients with overweight and obesity. A combination of a β-blocker (BAB) with a diuretic (D) (bisoprolol 2.5, 5, 10 mg and indapamid 1.5–2.5 mg/day) was prescribed to 102 patients with essential hypertension of 1–3 grades, 30 to 65 years old (mean age – 54.54 ± 0.91 years), who previously had not been receiving regular antihypertensive therapy. The daily dose of bisoprolol was administered by continuous slow titration, starting with low doses of 1.25 mg/day. Of the patients 82 were women and 20 men, the duration of disease averaged 9.0 ± 0.71 years. The control group included 16 healthy subjects matched for age and sex. The level of stable terminal metabolites of nitric oxide NO (nitrite NO2– and nitrate NO3–), the concentration of S-nitrosothiol and NO-synthases (NOS), SOD, and catalase activity was determined biochemically. The contents of serum 8-iso-PgF2α (8-isoprostane), TNF-alpha and its type I soluble receptor (sTNF-αRI) were determined in all subjects using the “8-isoprostane ELISA” (Usbiological,USA), “ProCon TNFα” (ProteinContour,Russian Federation) and “sTNF-RI EASIA” (BioSource Europe SA,Belgium) ELISA kits, respectively. During the course of combined antihypertensive therapy we observed a significant decrease of S-nitrosothiols levels, i-NOS activity, reduction of TNF-α type I of its soluble receptor (sTNF-αRI), and oxidative stress marker – 8-iso-PgF2α in the examined patients. Nitrites and nitrates serum levels, activity of e-NOS, superoxide dismutase and catalase, by contrast, were increased in patients with hypertension and concomitant obesity. These changes may reflect the fact that against the background of the therapy there was a reduction in tension of oxidative stress, which leads to an improvement in endothelial function. Significant reduction ratio of TNF-α/sTNF-αRI shows suppression of autoimmune and apoptotic activity in patients under treatment. Thus, the improvement of endothelial function, a significant decrease in autoimmune activation due to lower tension of oxidative stress in the examined patients optimizes use of a combination of bisoprolol and indapamid for differentiated therapy in hypertensive patients with obesity. 

The protective effects of carvacrol and thymol against paracetamol–induced toxicity on human hepatocellular carcinoma cell lines (HepG2)

2016 ◽  
Vol 35 (12) ◽  
pp. 1252-1263 ◽  
Author(s):  
SS Palabiyik ◽  
E Karakus ◽  
Z Halici ◽  
E Cadirci ◽  
Y Bayir ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Cytokines ◽  
Hepg2 Cells ◽  
Folk Medicine ◽  
Hepatoprotective Activity ◽  
High Dose ◽  
Protective Effects ◽  
And Oxidative Stress ◽  
Pro Inflammatory Cytokines

Acetaminophen (APAP) overdose could induce liver damage and lead to acute liver failure. The treatment of APAP overdoses could be improved by new therapeutic strategies. Thymus spp., which has many beneficial effects and has been used in folk medicine, is one such potential strategy. In the present study, the hepatoprotective activity of the main constituents of Thymus spp., carvacrol and thymol, were evaluated in light of APAP-induced hepatotoxicity. We hoped to understand the hepatoprotective mechanism of these agents on the antioxidant system and pro-inflammatory cytokines in vitro. Dose-dependent effects of thymol and carvacrol (25, 50, and 100 µM) were tested on cultured HepG2 cells. N-Acetylcysteine (NAC) was tested as positive control. We showed that APAP inhibited HepG2 cell growth by inducing inflammation and oxidative stress. Incubating APAP-exposed HepG2 cells with carvacrol and thymol for 24 h ameliorated this inflammation and oxidative stress. We also evaluated alanine transaminase and lactate dehydrogenase levels of HepG2 cells. We found that thymol and carvacrol protected against APAP-induced toxicity in HepG2 cells by increasing antioxidant activity and reducing pro-inflammatory cytokines, such as tumor necrosis factor α and interleukin 1β. Taking together high-dose thymol and carvacrol treatment has an effect close to NAC treatment in APAP toxicity, but thymol has better treatment effect than carvacrol.

Mitigation of IL-1β, IL-6, TNF-α, and markers of apoptosis by ursolic acid against cisplatin-induced oxidative stress and nephrotoxicity in rats

2021 ◽  
Vol 40 (12_suppl) ◽  
pp. S397-S405
Author(s):  
Pankaj Tripathi ◽  
Saeed Alshahrani
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Uric Acid ◽  
Inflammatory Cytokines ◽  
Caspase 3 ◽  
Caspase 9 ◽  
Histological Damage ◽  
Tnf Α ◽  
Mda Content ◽  
Pro Inflammatory Cytokines

Background: Ursolic acid (UA) is a natural pentacyclic triterpenoid that is known for its benefits under several pathological conditions. Cisplatin (CP) is among the most preferred chemotherapeutic agents; however, its nephrotoxicity limits its clinical utility. Purpose: This study was aimed to determine the role of UA in the reduction of CP-induced nephrotoxicity and mitigation of pro-inflammatory cytokines and apoptosis in a rat model. Methodology: Male Wistar rats were randomized into vehicle control, CP (7.5 mg/kg), UA 10 mg/kg, and CP with UA 5 and 10 mg/kg groups. Kidney and blood samples were collected for assessment of renal function, measurement of pro-inflammatory cytokines, apoptosis markers, antioxidant activity, and tissue histology. Results: CP significantly increased the levels of serum Cr, BUN, and uric acid; it also induced histological damage reflecting the pathophysiology observed during nephrotoxicity. CP has also shown its pro-oxidant activity in kidney tissue because CP decreased the levels of GSH, SOD, and CAT; it increased the lipid peroxidation as measured by MDA content. In addition, CP significantly upregulated the activity of pro-inflammatory cytokines and expression of apoptotic markers, that is, there were increased levels of IL-1β, IL-6, TNF-α, caspase-3, and caspase-9. Two weeks of continuous treatment of UA showed significant recovery against CP-induced nephrotoxicity; UA decreased the levels of Cr, BUN, and uric acid and ameliorated histological damage. UA also downregulated the activities of IL-1β, IL-6, and TNF-α as well as expression of caspase-3 and caspase-9. Furthermore, CP-induced oxidative stress that was antagonized by UA—the levels of GSH, SOD, and CAT were significantly increased while MDA content was decreased. Conclusions: UA has a protective effect against CP-induced nephrotoxicity, which may be due to its antioxidant activity and mitigation of ILβ-1, ILβ-6, TNF-α, and markers of apoptosis.

Etanercept Improves Lipid Profile and Oxidative Stress Measures in Patients with Juvenile Idiopathic Arthritis

2013 ◽  
Vol 40 (6) ◽  
pp. 943-948 ◽  
Author(s):  
Sara De Sanctis ◽  
M. Loredana Marcovecchio ◽  
Stefania Gaspari ◽  
Marianna Del Torto ◽  
Angelika Mohn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Juvenile Idiopathic Arthritis ◽  
Disease Activity ◽  
Lipid Profile ◽  
Proinflammatory Cytokines ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Oxidative Stress Marker ◽  
Tnf Α ◽  
And Oxidative Stress

Objective.To investigate the effect of 1-year treatment with the anti-tumor necrosis factor-α (TNF-α) drug etanercept on lipid profile and oxidative stress in children and adolescents with juvenile idiopathic arthritis (JIA).Methods.Thirty children with JIA (22 females; mean age 12.3 ± SD 5.7 yrs), all eligible for anti-TNF-α treatment, were assessed at baseline and after 6- and 12-month treatment with etanercept. Disease activity was determined using the Juvenile Arthritis Disease Activity Score (JADAS). Blood samples were drawn to measure the acute-phase reactants C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), lipids, and the proinflammatory cytokines TNF-α, interleukin-1β (IL-1β), IL-6 and interferon-γ. To measure the oxidative stress marker 8-iso-prostaglandin F2α, 24-h urine samples were collected.Results.Inflammatory indicators (CRP and ESR) and JADAS scores improved significantly after 1 year of etanercept treatment (all p < 0.001). Proinflammatory cytokines showed significant reduction during the study period (all p < 0.001). Similar reductions were detected in total cholesterol (p < 0.001), low-density lipoprotein cholesterol (p = 0.04), and triglycerides (p < 0.001), whereas no significant change was found in high-density lipoprotein cholesterol. No side effects were observed during the treatment period.Conclusion.This study shows for the first time that anti-TNF-α therapy for JIA is associated not only with a beneficial effect on clinical disease activity and inflammatory indexes, but also with improved lipid profile and oxidative stress. These findings suggest that TNF-α blockers might reduce atherosclerotic risk in children with JIA.

P941Acute effects of electronic hookah smoking on endothelial function, inflammation and oxidative stress

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Rezk-Hanna ◽  
E Ricci ◽  
E Ikharo ◽  
M L Brecht
Keyword(s):  
Oxidative Stress ◽  
Mean Arterial Pressure ◽  
Vitamin C ◽  
Endothelial Function ◽  
Acute Effect ◽  
Plasma Nicotine ◽  
Tnf Α ◽  
Before And After ◽  
Hookah Smoking ◽  
And Oxidative Stress

Abstract Background Electronic nicotine delivery systems (ENDS) are a new rapidly growing global epidemic. More recently, electronic (e-) hookahs, have increased in popularity in the United States, with the greatest uptake by young female adults, who endorse marketing claims that these products are safer alternatives to traditional hookah tobacco smoking. Unlike other ENDS such as e-cigarettes, e-hookah bowls are used through traditional waterpipes, allowing the vapor–containing aerosolized nicotine, propylene glycol, glycerin, and flavorings–to pass through a water-filled basin, before it is inhaled through the user's mouth. Contributing to e-hookah bowls' popularity is the belief that e-hookah flavored smoke is detoxified as it passes through the water-filled basin, rendering e-hookah a safer tobacco alternative. However, an e-hookah bowl delivers flavored nicotine by creating a vapor of fine (<2.5 μm) and ultrafine particles (<0.1 μm) that could induce vascular toxicity. Purpose To test the acute effect of electronic hookah smoking on endothelial function, inflammation and oxidative stress. Methods In 17 healthy young adults who smoke hookah but not cigarettes (age 26±1 years, mean±SE; BMI 23.8±0.7 kg-m2), we measured brachial artery flow-mediated dilation (FMD) before and after a 30-minute e-hookah bowl smoking. To test for inflammatory mediation, pro-inflammatory cytokines hsCRP, TNF-α, and fibrinogen were collected before and after smoking. To test for oxidative stress mediation, on a separate day, the acute effect of e-hookah smoking on FMD was examined after intravenous infusion of Vitamin C, an effective antioxidant. Plasma nicotine levels were collected before and after the smoking session. The same measurements were performed before and after a subset of subjects (n=8) performed a sham-smoking control study. Results E-hookah smoking, which markedly increased plasma nicotine (Δ plasma nicotine: +6.07±1.87, p=0.018) and mean arterial pressure (Δ mean arterial pressure: +12±2 mm Hg, p<0.001), acutely decreased FMD from 8.04±0.68 to 6.14±0.52%Δ, p<0.001, indicating impaired endothelial function. While fibrinogen and TNF-α levels increased from 225.31±7.41 to 236.77±9.79, p=0.026 and from 0.80±0.04 to 0.87±0.05, p=0.036, respectively, hsCRP did not change (P=ns). Vitamin C administration prevented the acute FMD impairment by e-hookah smoking (P=ns). All parameters were unchanged during sham-control studies. Conclusions In contrast to the widespread popular belief that e-hookah is safe, the data herein show that each e-hookah session constitutes a potent vascular toxin acutely impairing endothelial function and inducing an inflammatory state. That the acute impairment in FMD with electronic hookah is restored with administration of the potent antioxidant Vitamin C suggest that elevated vascular oxidative stress as a key mechanism involved. These new data provide evidence to counter claims that e-hookah is a safer tobacco alternative. Acknowledgement/Funding This work was funded by the National Institutes of Health, National Heart, Lung, and Blood Institute 1R21HL145002-01 to MRH.

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