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Abstract: TH-PO865

Astaxanthin Attenuates Diabetic Kidney Injury Through Up-Regulation of Autophagy

Session Information

Category: Diabetic Kidney Disease

  • 601 Diabetic Kidney Disease: Basic


  • Zhengyue, Chen, Ningbo Urology and Nephrology Hospital, Ningbo, China

The aim of this study was to investigate effects of astaxanthin (ATX) on renal injury in diabetic mice and its underlined renal protective mechanism.


Rats were randomly divided into five groups: normal, high fat diet, high fat + DM, high fat + ATX treatment, high fat + DM + ATX treatment. Fasting blood glucose,Urinary protein / Crea were measured. Renal pathological changes were evaluated with HE and PAS staining. In vitro, HTECs, HMCs and Podocytes were treated with ATX in the presence or absence of 30 mmol/L D-glucose or autophagy inducer.


Diabetic rats treated with ATX had reduced 24h urinary protein excretion, blood glucose and lipids level as compared with those in vehicle-treated rats. The same as Glomerulus mesangial matrix expansion and renal tubular epithelial cell injury(Fig1,2). Moreover, ATX treatment markedly reduced protein levels of p62, α-SMA, FN and collagen IV in the kidney of diabetic rats(Fig3). In vitro, high glucose was shown to inhibit expression LC3-II and increase expression of p62 as compared with normal glucose while these changes were reversed with ATX treatment. ATX treatment also inhibited expression of α-SMA, collagen IV and FN in cultured kidney cells(Fig4,5).


The current study shows that ATX attenuates diabetes-induced kidney injury probably through upregulation of autophagic activity in kidney cells and anti-fibrosis effects.

Figure 1. ATX treatment decrease serum glucose and urinary protein in diabetic rats. Fasting blood glucose,Urinary protein / Crea, H&E and PAS staining were measured. Figure 2. ATX reduces the expression of α-SMA , FN and collagen IV in the renal of diabetic rats.Figure 3. ATX induces autophagy in the renal of diabetic rats. Protein expression of α-SMA and FN in renal was determined by WB. Figure 4. ATX reduce renal fibrosis factors of HTECs, HMCs and Podocytes.Figure 5. ATX induces autophagy in HTECs A., HMCs B., Podocytess C..


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