Abstract
To evaluate the protective effects of α-lipoic acid on the kidneys of Goto-Kakisaki (GK) diabetic rats, ten GK diabetic rats were randomly divided into a diabetic control group and a lipoic acid-treated diabetic group with α-lipoic acid 35 mg·Kg−1 intraperitoneal injections. Four healthy Wistar rats served as normal controls. Malonaldehyde (MDA), ascorbic acid (vitamin C), vitamin E, glutathione (GSH) and superoxide dismutase (SOD) levels in renal homogenate, and urine protein excretion were measured. The expression of mRNA for NF-κB, NADPH oxidase subunits p22phox and p47phox in renal tissue was examined by realtime PCR. Pathological changes in renal tissue were evaluated by light and electron microscopy. There were significant increases in urine protein excretion, MDA levels and the expression of mRNA of NF-κB, p22phox and p47phox, and significant decreases in GSH, SOD, vitamin C and vitamin E levels in the diabetic control group compared with the normal control group. Pathological changes of renal tissue were more progressive in the diabetic control group than in the normal control group. All the parameters above were improved in the α-lipoic acid-treated diabetic group. Oxidative stress is increased in the kidney of type 2 diabetic GK rats. It is associated with the progression of diabetic nephropathy. α-lipoic acid can protect renal function in diabetic rats via its antioxidant activity.
Highlights
Diabetic nephropathy is a severe, chronic complication of type 2 diabetes mellitus, and it is the main cause of end-stage renal failure in diabetic patients [1]
Compared to the normal control group, blood glucose levels were significantly increased in the two diabetic groups there was no significant difference in blood glucose levels between the diabetic control group and the ALA-treated diabetic group (Figure 1 and Table 1)
Compared to the normal control group, body weight was decreased in the diabetic control group
Summary
Diabetic nephropathy is a severe, chronic complication of type 2 diabetes mellitus, and it is the main cause of end-stage renal failure in diabetic patients [1]. The increased oxidative stress leads to injuries of the glomeruli [4], tubular interstitial tissue [5] and vasculature [6]. It is implicated in the mesangial expansion of extra-cellular matrix, and results in increases in glomerular filtration rate, urine protein excretion, progression of glomerular sclerosis and tubular-interstial fibrosis [7,8,9]. In light of the antioxidant activity of ALA, the purpose of this study was to verify oxidative stress in the pathogenesis of diabetic nephropathy in type 2 diabetic rats and to evaluate the protective effect of ALA on diabetic nephropathy
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