10.6084/m9.figshare.4750999.v1
Deshmukh A.B.
Deshmukh
A.B.
Patel J.K.
Patel
J.K.
Mishra B.
Mishra
B.
Supplementary Material for: Investigating the Effect of CoCl2 Administration on Diabetic Nephropathy and Associated Aortic Dysfunction
Karger Publishers
2017
Chronic hypoxia
Hypoxia inducible factor-1α
Prolyl hydroxylase
Oxidative stress
Nitric oxide
Angiotensin II
Endothelial dysfunction
2017-03-14 13:02:37
Dataset
https://karger.figshare.com/articles/dataset/Supplementary_Material_for_Investigating_the_Effect_of_CoCl2_Administration_on_Diabetic_Nephropathy_and_Associated_Aortic_Dysfunction/4750999
<strong><em>Aim:</em></strong> Endothelial dysfunction appears to be a consistent finding in diabetic nephropathy. The study aimed to investigate the effect of cobalt chloride in the amelioration of endothelial dysfunction in uninephrectomized diabetic rats. <b><i>Methods:</i></b> We examined the effect of CoCl<sub>2</sub> (10 mg/kg, i.p., OD = once a day) treatment on contractile responses to angiotensin II (10<sup>–10</sup> to 10<sup>–6</sup>M) in an aortic preparation of control rats and uninephrectomized diabetic control rats. Blood glucose, plasma urea, creatinine, uric acid, aortic endothelial nitric oxide synthase (eNOS), nitrate/nitrite (NOx), superoxide dismutase, catalase and reduced glutathione levels were checked in the different groups. <b><i>Results:</i></b> A significant attenuation of the augmented responses to angiotensin II was observed in CoCl<sub>2</sub>-treated animals along with a fall in plasma urea, creatinine and uric acid levels. A significant reduction in blood glucose and an increase in aortic eNOS and NOx levels along with antioxidants levels were observed. <b><i>Conclusion: </i></b>Chronic hypoxia augments angiotensin II responses in the thoracic aorta of uninephrectomized diabetic control rats. CoCl<sub>2</sub> attenuates these enhanced vascular responses with a significant decrease in blood glucose signifying stabilization of the hypoxia-inducible factor in the alleviation of endothelial dysfunction in diabetic nephropathy.