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1.
Artigo | IMSEAR | ID: sea-190011

RESUMO

Globally, one of the major causes of mortality and morbidity is ischemic heart disease (IHD). It has been established that in cardiac disorders, there exists a synergistic correlation between the oxidative stress and inflammatory cytokines. The stabilization and regulation of the oxidative stress and inflammatory cytokines in these patients is essential for the better management of the disease. Hence, the aim of this study was to study the effect of natural antioxidant, resveratrol, on the oxidative stress and inflammatory biomarkers in cultures of monocytes isolated from peripheral blood mononuclear cells (PBMCs) from the patients with myocardial infarction. Monocytes isolated from peripheral blood mononuclear cells (PBMC’s) of patients with myocardial infarction (MI) and healthy controls were employed in culture studies (with and without resveratrol). The 24 h cultures were subjected to evaluation of cytokine/ interleukins levels i.e. TNF-α, IL-1 and IL-6 as well as oxidative stress markers like MDA and Glutathione. The patient’s samples exhibited a significantly decreased level of intramonocyte glutathione as compared to samples of healthy subjects. On the other hand, significantly increased levels of MDA were observed in culture supernatants of monocytes isolated from PBMC’s of patients with MI in comparison to those of healthy controls. A significant degree of amelioration in intramonocyte glutathione levels coupled with decreased MDA levels (culture supernatants) were observed in cultures treated with resveratrol (20 ug/mL). Furthermore, 24 h culture supernatants of untreated patients cells exhibited augmented levels of IL-1, IL-6, and TNF-α. However, co-culturing with resveratrol exhibited a significant decrease in the levels of all the IL-1, IL-6 and TNF-α. Resveratrol—a potent polyphenol from grapes and also a natural antioxidant regulates the oxidative stress and inflammatory biomarkers and may be used as a prophylactic antioxidant in high risk patients.

2.
Indian J Physiol Pharmacol ; 2015 Jul-Sept; 59(3): 341-345
Artigo em Inglês | IMSEAR | ID: sea-179467

RESUMO

COPD has widespread systemic manifestations. Inflammation plays important role in its pathophysiology. Aim of the present study was to compare markers of oxidative stress and inflammation between obese and non obese COPD patients. The levels of pro inflammatory cytokines CRP, IL6 and TNF α were compared between obese and non-obese subjects by applying student’s t test. Oxidative imbalance was assessed by analyzing MDA and FRAP assay in same subjects. Correlation of BMI with the above study parameters was analyzed using Pearson’s test. Results indicated that levels of CRP, IL6 and TNF α were elevated in obese group as compared to non-obese group (p<0.001). Total antioxidant capacity estimated by FRAP assay was lower (p=0.005) but the levels of oxidants estimated indirectly by MDA was higher (p=0.01) in obese COPD patients. In all COPD patients included in present study BMI correlated inversely with FRAP (r=-0.546, p=0.013), FVC (r=0.548, p=0.012) and FEV1 (r=-0.865, p<0.001). Similarly BMI correlated positively with markers of inflammation namely CRP(r=0.526, p=0.017), IL6(r=0.865, p<0.001), TNF α (r=0.653,p=0.002). Positive correlation of BMI was found with MDA(r=0.536, p=0.015). Conclusion: there is higher inflammation in obesity resulting in oxidant antioxidant imbalance and lung function decline.

3.
Indian J Physiol Pharmacol ; 2012 Oct-Dec; 56(4): 345-352
Artigo em Inglês | IMSEAR | ID: sea-146131

RESUMO

Chronic Obstructive Pulmonary Disorder (COPD) is projected to rank third leading cause of deaths by 2030 as per WHO. COPD is a multietiological disease. The airflow dysfunction is usually progressive, associated with an abnormal inflammatory response of the lungs to noxious particles or gasses. As the lung is exposed to high levels of oxygen, it is more susceptible to oxidants mediated injury. Gender based differences are identifiable risk factors. Smoking is found to be a major risk factor in the causation of COPD resulting in oxidative stress . The aim of the present study is to evaluate the oxidant antioxidant imbalance in healthy non smoker controls and smokers with COPD. A total of 60 control (healthy non smokers) and 121 smokers having COPD were studied. The mean age is more in smoker group as compared to healthy controls, which identifies advancing age as a risk factor for COPD. The mean BMI and weight of smoker group is reduced as compared to control group. GOLD 2008 criteria was used to assess lung functions. Lung functions namely FEV1, FVC, FEV1/FVC% and FEV1% Predicted showed significant reduction in smoker group as compared to healthy non smoker controls. MDA in control and smoker group (1.09±0.09 and 1.41±0.23 nmol/ml respectively) showed significant changes (P<0.001). Our results also demonstrate significant reduction in anti oxidant enzymes namely SOD (units/mg of serum protein), Catalase (units/mg of serum protein) and GPX (nmol of NADPH oxidized/ min/mg of serum protein) in smoker group as compared to healthy controls. On the basis of study it is concluded that smoking, gender and oxidant antioxidant imbalance are identifiable risk factors in COPD.

4.
Artigo em Inglês | IMSEAR | ID: sea-172039

RESUMO

Apoptotic effects of curcumin (diferuloyl methane) on squamous cell carcinoma of the cervix. The present study was conducted in departments of Pathology and Biochemistry, JNMC, AMU, over a period of one and half yrs. Caspase-3 and TNF-alpha assay was performed on monocytes isolated from cervical carcinoma patients and cultured with curcumin; cytosmears and sections from cervical carcinoma tissue cultured with curcumin were prepared for the morphological evidence of apoptosis. Curcumin in the doses of 500 microg/ml increased the caspase-3 levels and decreases the level of TNF-alpha in human cells. Cytosmears and sections from cervical carcinoma tissue cultured with curcumin showed better differentiation and increased number of apoptotic cells as compared to non curcumin controls. Curcumin in a dose of 500 microg/ ml promoted apoptotic preparedness of human cells and induced apoptotic change in cervical carcinoma cells.

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