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.
"Diosgenin(Dio), a naturally occurring steroid saponin, is abundantly produced in yam tubers (Dioscorea sp.) and fenugreek seeds (Trigonella sp.)5. Over the past three decades, Dio has primarily been studied for the prevention and/or treatment of various diseases, such as cancer6, diabetes7, obesity8, and dyslipidemia9. Moalic et al showed that Dio inhibits leukemia and the growth of various cell lines from solid tumors in vitro and in vivo10,11,12. "
[Show abstract][Hide abstract] ABSTRACT: Aim:
To investigate the effects of diosgenin (Dio), a naturally occurring steroid saponin, on goiter formation in a mouse model of Graves' disease (GD) and the underlying mechanisms.
Female BALB/c mice were injected with adenovirus expressing the A subunit of thyrotropin receptor to induce GD. The mice were treated with Dio (20, 100 mg·kg−1·d−1, ip) for 12 or 24 d. The serum levels of TT4 and TRAb were examined using radioimmunoassay and electrochemiluminescence. The size and morphology of thyroid glands were examined. Thyrocyte proliferation was determined using BrdU incorporation assay. The expression of proliferation-associated proteins IGF-1, NF-κB, cyclin D1, and PCNA in thyroids was analyzed using immunohistochemistry and real-time PCR.
The GD mice showed significantly high serum levels of TRAb and TT4 compared to the normal mice. Treatment of the GD mice with Dio for 24 d dose-dependently reduced the TT4 level and thyroid size, but did not affect the abnormal level of TRAb. Furthermore, Dio treatment dose-dependently reversed the morphological changes and reduced excessive thyrocyte proliferation in thyroids of the GD mice. Dio treatment also dose-dependently reduced the mRNA and protein levels of IGF-1, NF-κB, cyclin D1, and PCNA in thyroids of the GD mice.
Dio relieves goiter in a mouse model of GD through the inhibition of thyrocyte proliferation. The mechanisms involve the suppression of IGF-1, NF-κB, cyclin D1, and PCNA expression.
"Studies have also suggested a lower incidence for coronary artery diseases and disorders related to estrogen deficiencies in humans who have a high consumption of diet rich in phytoestrogens (i.e., genistein, daidzein, and diosgenin) . Recent studies discovered that diosgenin have antioxidant potential and inhibits the production of intracellular ROS species, aortic remodeling, vascular calcification and lipid peroxidation  . There was a strong link between oxidative stress, tissue abnormalities and renal failure. "
[Show abstract][Hide abstract] ABSTRACT: The aim of the present study was to evaluate the effect of diosgenin a proven
antioxidant on chronic renal failure (CRF) induced abnormalities linked with oxidative stress
in heart. CRF was induced in male Wistar rats by feeding the animals with 0.75% adenine-containing diet and diosgenin was given orally (everyday at the dose of 40 mg/kg). Effect of
diosgenin on cardiac tissue lipids, trace elements (iron, zinc, magnesium, copper and
manganese) and activity of cardiac mitochondrial enzymes were assayed. Expression of
tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) was also assessed. The Fourier
transform infrared spectroscopy (FTIR) analysis was employed to indicate the oxidative
stress related molecular changes in heart tissue. The outcomes of the study indicated that,
diosgenin reduces the tissue lipid abnormalities induced by CRF. Cardiac elemental
concentration was not changed in all groups but the plasma zinc was altered and diosgenin
have no effect on it. Cardiac mitochondrial enzymes abnormalities and proinflammatory
cytokines expression was also significantly reduced by diosgenin. Finally, the molecular and
structural changes of proteins were also reduced by diosgenin treatment. The overall study
shows that diosgenin with antioxidant function have enough potential to improve cardiac
Biomedicine and Preventive Nutrition 08/2013; DOI:10.1016/j.bionut.2013.08.005
[Show abstract][Hide abstract] 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.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.