ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: TH-PO865

Astaxanthin Attenuates Diabetic Kidney Injury Through Up-Regulation of Autophagy

Session Information

Category: Diabetic Kidney Disease

  • 601 Diabetic Kidney Disease: Basic

Author

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

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

Methods

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.

Results

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).

Conclusion

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..

Funding

  • Government Support - Non-U.S.