Beneficial role of diosgenin on oxidative stress in aorta of streptozotocin induced diabetic rats.
ABSTRACT The present study was designed to investigate the beneficial role of diosgenin on oxidative stress markers and histopathological changes in aorta of streptozotocin induced diabetic rats. Diabetes was induced in experimental rats by a single intraperitoneal injection of streptozotocin (55 mg/kg body weight (b.w.)). From the sixth week, experimental rats received diosgenin at different doses (10, 20 and 40 mg/kg b.w.) once daily for 4 weeks. At the end of the experimental periods, diabetic rats exhibited significant increase in the levels of plasma glucose, glycosylated hemoglobin with significant decrease in insulin and total hemoglobin. The activities of antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase and the levels of reduced glutathione were decreased while increases in the levels of lipid peroxidation markers were observed in aortic tissues of diabetic rats. Oral administration of diosgenin to diabetic rats significantly decreased the plasma glucose and increased the insulin level based on a dose dependent manner. Diosgenin at a dose of 40 mg/kg b.w. was more pronounced effect than the other two doses and used for further studies. All the manifestations observed in diabetic rats were significantly reversed to near normal at a dose of 40 mg/kg b.w. of diosgenin. These findings suggest that diosgenin could have a beneficial role against aortic damage induced by oxidative stress in diabetic state, which was evidenced by the propensity of diosgenin to modulate the antioxidant defense and to decrease the lipid peroxidation in aorta.
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ABSTRACT: In recent years, the role of endothelial dysfunction (ED) and excessive oxidative stress in the development of cardiovascular diseases has been highlighted. The aim of the present study is to evaluate the effect of diosgenin, an antioxidant on chronic renal failure (CRF) induced vascular dysfunction. CRF was induced by feeding the rats with a diet containing 0.75 % adenine and diosgenin was given orally (everyday at the dose of 40 mg/kg). Isometric force measurement was performed on isolated aortic rings in organ baths. Levels of reduced glutathione (GSH), nitric oxide metabolites, and endothelial nitric oxide synthase mRNA in rat aorta were examined. Further, plasma lipid profile, activity of enzymes of lipid metabolism, and aortic angiotensin converting enzyme (ACE) also studied. The overall results have proved that diosgenin attenuates CRF-induced impairment in acetylcholine induced endothelium-dependent and sodium nitroprusside induced endothelium-independent vascular relaxation. Moreover, it elevates the GSH and restores the eNOS mRNA expression level. CRF-induced dyslipidemia and ACE activity was also inhibited by diosgenin treatment. This study indicates that diosgenin have enough potential to protect vasculature against oxidative stress, dyslipidemia which in turn improves the vascular function in CRF milieu.Molecular and Cellular Biochemistry 08/2013; · 2.33 Impact Factor
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ABSTRACT: Vascular calcification due to elevated phosphate levels is the major contributor of cardiovascular dysfunction. The oxidative stress and gene expression events modulate the transdifferentiation of vascular smooth muscle cells into osteogenic phenotype. This present study intends to evaluate the dose-dependent effect of diosgenin, an antioxidant on high phosphate induced vascular calcification in adenine-induced chronic renal failure rats. High phosphate environment causes elevated calcium accumulation with related histological changes and alkaline phosphatase activity in aorta. Further it downregulates the activity of enzymatic antioxidants and elevates the level of lipid peroxidative markers. Moreover, the renal failure leads to reduced nitric oxide production. But, treatment with diosgenin at a dose of 10, 20, and 40 mg/kg given via oral gavages causes reversion of all the above events in a dose-dependent manner. The highest dose has shown more potential activity than other two doses, which has the ability to protect the alteration of liver markers and red blood cell antioxidant system without any adverse effects and it does not alter the kidney associated changes too. Finally, the Fourier transform infrared spectroscopy study strongly supports its ability to protect the macromolecules from oxidative stress. All the above evidences show that diosgenin has overall benefits against renal failure-induced vascular calcification-associated oxidative stress.Molecular and Cellular Biochemistry 02/2013; · 2.33 Impact Factor
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ABSTRACT: Reperfusion injury is one of the main reasons of cardiac disease morbidity. Phytopharmaceuticals are gaining importance in modern medicine of cardioprotection because of their multiplex capacity. The aim of this study was to investigate the effect of diosgenin on the inflammatory response induced by myocardial ischemia and reperfusion injury and the role of mitochondrial ATP-sensitive potassium (mitoKATP) channels in this regard. Wistar rats (250-300 g) were used in this study. The Langendorff-perfused hearts of animals were subjected to a 30-min global ischemia followed by a 90-min reperfusion. The lactate dehydrogenase (LDH) release was measured by spectrophotometry. The levels of inflammatory mediators tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), and IL-6 in the supernatant of heart's left ventricle were measured using an enzyme-linked immunosorbent assay rat specific ELISA kit. The LDH release into the coronary effluent during reperfusion was significantly decreased, and cardiac contractility significantly improved by diosgenin preadministration as compared with those of control or Cremophor-EL (solvent of diosgenin) groups (398 ± 48 vs. 665 ± 65 or 650 ± 73 ml/min) (P < 0.01). Administration of diosgenin before the main ischemia significantly reduced the levels of IL-6 (P < 0.05), IL-1β, and TNF-α (P < 0.01) in the reperfusion phase of diosgenin-treated hearts as compared with untreated control hearts. Inhibition of mitoKATP channels by 5-hydroxydecanoate significantly reverses the cardioprotective effects of diosgenin (P < 0.05). The findings of the present study indicate that preconditioning with diosgenin may induce cardioprotective effect against reperfusion injury through reducing the production of inflammatory mediators and activating the mitoKATP channels.Journal of physiology and biochemistry 02/2014; · 1.65 Impact Factor