Oxidative stress is implicated as an important mechanism by which diabetes causes nephropathy.
Astaxanthin, which is found as a common pigment in algae, fish, and birds, is a
carotenoid with significant potential for antioxidative activity. In this study, we examined whether chronic administration of
astaxanthin could prevent the progression of
diabetic nephropathy induced by oxidative stress in mice. We used female db/db mice, a rodent model of
type 2 diabetes, and their non-diabetic db/m littermates. The mice were divided into three groups as follows: non-diabetic db/m, diabetic db/db, and diabetic db/db treated with
astaxanthin.
Blood glucose level,
body weight, urinary
albumin, and urinary
8-hydroxydeoxyguanosine (8-OHdG) were measured during the experiments. Histological and 8-OHdG immunohistochemical studies were performed for 12 weeks from the beginning of treatment. After 12 weeks of treatment, the
astaxanthin-treated group showed a lower level of
blood glucose compared with the non-treated db/db group; however, both groups had a significantly high level compared with the db/m mice. The relative mesangial area calculated by the mesangial area/total glomerular area ratio was significantly ameliorated in the
astaxanthin-treated group compared with the non-treated db/db group. The increases in urinary
albumin and 8-OHdG at 12 weeks of treatment were significantly inhibited by chronic treatment with
astaxanthin. The 8-OHdG immunoreactive cells in glomeruli of non-treated db/db mice were more numerous than in the
astaxanthin-treated db/db mice. In this study, treatment with
astaxanthin ameliorated the progression and acceleration of
diabetic nephropathy in the rodent model of
type 2 diabetes. The results suggested that the antioxidative activity of
astaxanthin reduced the oxidative stress on the kidneys and prevented renal cell damage. In conclusion, administration of
astaxanthin might be a novel approach for the prevention of diabetes nephropathy.