Boobalan Raja

Veratric acid, a phenolic acid attenuates blood pressure and oxidative stress in L-NAME induced hypertensive rats.

The present study was undertaken to assess the antihypertensive and antioxidant effects of veratric acid on N(ω)-nitro-L arginine methyl ester (L-NAME) induced hypertensive rats. Hypertension was induced in adult male albino rats of the Wistar strain, weighing 180-220 g, by oral administration of the L-NAME (40 mg/kg body weight/day) in drinking water for 4 weeks. Rats were treated with various doses of veratric acid (20, 40, 80 mg/kg/day) for four weeks. Hypertension was manifested by considerably increased systolic and diastolic blood pressure and the toxic effect of L-NAME was determined using lipid peroxidative markers (thiobarbituric acid reactive substances and lipid hydroperoxides). We also assessed the activities of enzymatic antioxidants (superoxide dismutase, catalase, and glutathione peroxidase) and measured the levels of non-enzymatic antioxidants (vitamin-C, vitamin-E and reduced glutathione) levels in erythrocytes, plasma and tissues and plasma nitric oxide metabolites (nitrite/nitrate). Oral administration of veratric acid at the dosage of 40 mg/kg considerably decreased systolic and diastolic blood pressure, lipid peroxidation products; increased plasma nitric oxide levels and showed no toxicity which was measured using hepatic and renal function markers when compared to other doses of veratric acid (20, 80 mg/kg). In addition, histopathological findings of veratric acid treated hypertensive rat heart confirmed the biochemical findings of this study. These results suggest that veratric acid decreased the blood pressure, significantly restored nitric oxide, enzymatic and non-enzymatic antioxidants and reduced lipid peroxidation products and thus exhibits antihypertensive and antioxidant effects against l-NAME induced hypertension.

Diosmin, a bioflavonoid reverses alterations in blood pressure, nitric oxide, lipid peroxides and antioxidant status in DOCA-salt induced hypertensive rats.

The present study was aimed to evaluate the antihypertensive effect of diosmin in deoxycorticosterone acetate (DOCA)-salt induced hypertension in male Wistar rats. Hypertension was induced in uninephrectomized rats by weekly twice subcutaneous injection of DOCA (25 mg/kg body weight) and 1% NaCl in the drinking water for six consecutive weeks. The important pathological events that occurred in DOCA-salt treated rats were significant increase in systolic, diastolic blood pressure, sodium and chloride in serum and lipid peroxidation products (thiobarbituric acid reactive substances, lipid hydroperoxides and conjugated dienes) in plasma and tissues (liver, kidney, heart and aorta) and significant decrease in serum potassium, total nitrite and nitrate levels in plasma. The activities of hepatic aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and gamma-glutamyl transpeptidase and the levels of renal urea, uric acid, creatinine in serum, water intake, and organ weight (kidney and heart) were significantly increased in DOCA-salt hypertensive rats. DOCA-salt treated rats also showed a significant decrease in body weight, activities of superoxide dismutase, catalase and glutathione peroxidase in erythrocyte and tissues and the levels of reduced glutathione, vitamin C and vitamin E in plasma and tissues. Treatment with diosmin (25, 50 and 100 mg/kg body weight) brings back all the above parameters to near normal level, in which 50 mg/kg body weight showed the highest effect than that of other two doses. Histopathology of heart and kidney also confirmed the protective effect of diosmin. Thus the experiment clearly showed that diosmin acts as an antihypertensive agent against DOCA-salt induced hypertension.

Antihypertensive and antioxidant potential of vanillic acid, a phenolic compound in L-NAME-induced hypertensive rats: a dose-dependence study.

Abstract We investigated the antihypertensive and antioxidant potential of vanillic acid (VA) in Nω-Nitro-l-arginine methyl ester hydrochloride (l-NAME) – treated adult male albino Wistar rats. Treatment of rats with l-NAME (40 mg/kg Bw for 30 days) caused a sustained increase in systolic- (SBP) and diastolic blood pressure (DBP) and significantly decreased the concentration of nitrite/nitrate (NOx) in plasma as compared with that in the control. Rats treated with VA restored SBP and DBP to normal level and preserve the plasma NO metabolites concentration. Moreover, VA reduced lipid peroxidation products (thiobarbituric acid reactive substances, lipid hydroperoxides, conjugated dienes) and significantly restored enzymatic antioxidants (superoxide dismutase, catalase, and glutathione peroxidase), non-enzymatic antioxidants (vitamin C, vitamin E, and reduced glutathione) in the plasma. To assess the toxicity if any of VA treatment, hepatic and renal function markers were measured. Our results showed that the effect at a dose of 50 mg/kg Bw of VA was more pronounced than that of the other two doses, 25 and 100 mg/kg Bw. These results were supported by histopathology studies. We conclude that VA possesses an antihypertensive and antioxidant activity in l-NAME-induced hypertensive rats.

Morin attenuates blood pressure and oxidative stress in deoxycorticosterone acetate-salt hypertensive rats: A biochemical and histopathological evaluation

The present study was designed to evaluate the antihypertensive and antioxidant effect of morin, a flavonoid against deoxycorticosterone acetate (DOCA)-salt induced hypertension in male Wistar rats. Hypertension was induced in uninephrectomized rats (UNX) by weekly twice subcutaneous injection of DOCA (25mg/kg) and 1% NaCl in the drinking water for six consecutive weeks. The DOCA-salt hypertensive rats showed significant (P < .05) increase in the systolic and diastolic blood pressure, heart rate, water intake and organ weights (kidney, heart, aorta and liver). DOCA-salt hypertensive rats also showed significant (P < .05) increase in the levels of thiobarbituric acid reactive substances, lipid hydroperoxides and conjugated dienes in plasma and tissues (kidney, heart, aorta and liver), and significant (P < .05) decrease in the body weight, nitrite and nitrate levels in plasma and heart. Furthermore, the activities of enzymic antioxidants such as superoxide dismutase, catalase and glutathione peroxidase in erythrocyte and tissues and the levels of non-enzymic antioxidants such as reduced glutathione, vitamin C and vitamin E in plasma and tissues were significantly (P < .05) decreased in DOCA-salt rats. Morin supplementation (50mg/kg) daily for six weeks brought back all the above parameters to near normal level. The above findings were confirmed by the histopathological examination. No significant (P < .05) effect was observed in UNX-rats treated with morin (50mg/kg). These results suggest that morin acts as an antihypertensive and antioxidant agent against DOCA-salt induced hypertension.

Sinapic Acid Prevents Hypertension and Cardiovascular Remodeling in Pharmacological Model of Nitric Oxide Inhibited Rats

Objectives Hypertensive heart disease is a constellation of abnormalities that includes cardiac fibrosis in response to elevated blood pressure, systolic and diastolic dysfunction. The present study was undertaken to examine the effect of sinapic acid on high blood pressure and cardiovascular remodeling. Methods An experimental hypertensive animal model was induced by L-NAME intake on rats. Sinapic acid (SA) was orally administered at a dose of 10, 20 and 40 mg/kg body weight (b.w.). Blood pressure was measured by tail cuff plethysmography system. Cardiac and vascular function was evaluated by Langendorff isolated heart system and organ bath studies, respectively. Fibrotic remodeling of heart and aorta was assessed by histopathologic analyses. Oxidative stress was measured by biochemical assays. mRNA and protein expressions were assessed by RT-qPCR and western blot, respectively. In order to confirm the protective role of SA on endothelial cells through its antioxidant property, we have utilized the in vitro model of H2O2-induced oxidative stress in EA.hy926 endothelial cells. Results Rats with hypertension showed elevated blood pressure, declined myocardial performance associated with myocardial hypertrophy and fibrosis, diminished vascular response, nitric oxide (NO) metabolites level, elevated markers of oxidative stress (TBARS, LOOH), ACE activity, depleted antioxidant system (SOD, CAT, GPx, reduced GSH), aberrant expression of TGF-β, β-MHC, eNOS mRNAs and eNOS protein. Remarkably, SA attenuated high blood pressure, myocardial, vascular dysfunction, cardiac fibrosis, oxidative stress and ACE activity. Level of NO metabolites, antioxidant system, and altered gene expression were also repaired by SA treatment. Results of in vitro study showed that, SA protects endothelial cells from oxidative stress and enhance the production of NO in a concentration dependent manner. Conclusions Taken together, these results suggest that SA may have beneficial role in the treatment of hypertensive heart disease by attenuating fibrosis and oxidative stress through its antioxidant potential.

Diosmin pretreatment improves cardiac function and suppresses oxidative stress in rat heart after ischemia/reperfusion

Reperfusion of ischemic tissue leads to the generation of oxygen derived free radicals which plays an important role in cellular damage. Objective of the current study is to evaluate the cardio-protective and antioxidant effect of diosmin on ischemia-reperfusion related cardiac dysfunction, oxidative stress and apoptosis. Diosmin (50 and 100 mg/kg body weight (bw)) was given every day to the rats orally throughout the experimental period. Ischemia/reperfusion protocol was carried out ex vivo using langendorff perfusion method and the cardiac functional recovery was assessed in terms of percentage rate pressure product. Coronary effluents of LDH and CK-MB activities, antioxidant enzyme activities, lipid peroxidation products, activity of TCA cycle enzymes were evaluated. Moreover, in vitro superoxide anion and hydroxyl radical scavenging potential of diosmin was also quantified. Finally, quantitative real-time PCR was used for assessing Bcl-2 mRNA expression in heart. Cardiac functional recovery was impaired after reperfusion compared with continuously perfused heart. It was significantly prevented by diosmin treatment. Impaired antioxidant enzyme activities and elevated lipid peroxidation products level were also significantly suppressed. The activity of TCA cycle enzymes was protected against reperfusion stress. Down regulated Bcl-2 was also significantly increased. This study concluded that diosmin pretreatment prevents all the impaired patterns including cardiac function, oxidative stress and apoptosis associated with reperfusion in control heart by its antioxidant role.

Effect of morin, a flavonoid against DOCA-salt hypertensive rats: a dose dependent study

OBJECTIVE To determine the protective effect of morin, a flavonoid against deoxycorticosterone acetate (DOCA)-salt induced hypertension in male Wistar rats. METHODS Hypertension was induced in uninephrectomized rats by weekly twice subcutaneous injection of DOCA (25 mg/kg bw) and 1% NaCl in the drinking water for six consecutive weeks. Effect of morin against DOCA-salt induced hypertension was evaluated by measuring blood pressure and performing biochemical estimations and histopathological examination of renal tissues. RESULTS DOCA-salt hypertensive rats showed considerably increased systolic and diastolic blood pressure, serum hepatic marker enzyme activities such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and gamma-glutamyl transpeptidase (GGT) and renal function markers (urea, uric acid and creatinine) in plasma. Oral administration of morin (25, 50 and 75 mg/kg bw) brought back all the above parameters to near normal level. Histopathology of kidney also confirmed the biochemical findings of this study. The effect at a dose of 50 mg/kg bw of morin was more pronounced than that of the other two doses (25 and 75 mg/kg bw). CONCLUSIONS These findings indicate that morin exhibits strong antihypertensive effect against DOCA-salt induced hypertension.

Evaluation of antioxidant activity of Melothria maderaspatana in vitro

In this study, an aqueous extract of leaves from Melothria maderaspatana was tested for in vitro antioxidant activity. Free radical scavenging assays, such as hydroxyl radical, hydrogen peroxide, superoxide anion radical and 2,2-diphenyl-1-picryl hydrazyl (DPPH), 2,2’-azinobis-(3-ethyl-enzothiazoline-6-sulfonic acid) (ABTS) radical scavenging, and reducing power assay, were studied. The extract effectively scavenged hydroxyl radical, hydrogen peroxide and superoxide anion radicals. It also scavenged DPPH and ABTS radicals. Furthermore, it was found to have reducing power. All concentrations of leaf extract exhibited free radical scavenging and antioxidant power, and the preventive effects were in a dose-dependent manner. The antioxidant activities of the above were compared to standard antioxidants such as butylated hydroxytoluene (BHT), ascorbic acid, and α-tocopherol. The results obtained in the present study indicate that the M. maderaspatana extract could be considered a potential source of natural antioxidant.

Sinapic acid protects heart against ischemia/reperfusion injury and H9c2 cardiomyoblast cells against oxidative stress

The present study was designed to evaluate antioxidant and cardioprotective potential of sinapic acid (SA) against ischemia/reperfusion (I/R) injury. Cardiac functional recovery after I/R was evaluated by percentage rate pressure product (%RPP) and percentage coronary flow (%CF). Myocardial injury was evaluated by 2,3,5-triphenyltetrazolium chloride (TTC) staining and LDH enzyme leakage. Oxidative stress was estimated by lipid peroxidation level. eNOS protein expression in reperfused heart was assessed using Western blot method. Finally, in order to support the antioxidant effect of SA, in vitro protective potential of SA was assessed on H2O2-induced oxidative stress in H9c2 cardiomyoblast cells. The overall results demonstrated that I/R induced cardiac dysfunction, injury and oxidative stress was attenuated by SA treatment. Moreover, in vitro results also shown that, SA protects H9c2 cells from oxidative stress and modulates mitochondrial membrane permeability transition (MPT). In conclusion, coupled results from both in vivo and in vitro experiments have confirmed that SA with antioxidant role protects cardiac cells and its functions from I/R induced oxidative stress.

Vanillic acid: a potential inhibitor of cardiac and aortic wall remodeling in l-NAME induced hypertension through upregulation of endothelial nitric oxide synthase.

The objective of the present study is to investigate the effects of vanillic acid on blood pressure, cardiac marker enzymes, left ventricular function and endothelial nitric oxide synthase (eNOS) expression in N(ω)-nitro-l-arginine methyl ester hydrochloride (l-NAME) induced hypertension in male albino Wistar rats. In hypertensive rats, mean arterial pressure (MAP), heart rate, cardiac marker enzymes and organ weight were increased. Impaired left ventricular function and decreased aortic eNOS expression was also observed in hypertensive rats. Moreover, treatment with vanillic acid exhibited beneficial effect on blood pressure, left ventricular function and cardiac marker enzymes. In addition, treatment with vanillic acid on hypertensive rats had upregulated eNOS expression and showed beneficial effects evidenced by histopathology and ultrastructural observations of aorta. In conclusion, vanillic acid has enough potential to normalize hypertension and left ventricular function in l-NAME induced hypertensive rats. With additional studies, vanillic acid might be used as a functional drug or as an adjuvant in the management of hypertension.