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Kidney Week

Abstract: TH-PO467

The Novel NQO1 Donor Reduced Renal Fibrosis in Unilateral Ureteral Obstruction Mice

Session Information

  • CKD: Mechanisms - I
    November 07, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: CKD (Non-Dialysis)

  • 2103 CKD (Non-Dialysis): Mechanisms

Authors

  • Choi, Dae Eun, Chungnam National University, Daejeon, Korea (the Republic of)
  • Hwang, Tae Woong, Chungnam National University, Daejeon, Korea (the Republic of)
  • Kim, Da bi, Chungnam National University, Daejeon, Korea (the Republic of)
  • Kim, Eunji, Chungnam National University, Daejeon, Korea (the Republic of)
  • Jeong, Jin young, Chungnam National University, Daejeon, Korea (the Republic of)
  • Kim, Jwajin, Chungnam National University, Daejeon, Korea (the Republic of)
  • Kim, Hae Ri, Chungnam National University, Daejeon, Korea (the Republic of)
  • Jeon, Jae wan, Chungnam National University, Daejeon, Korea (the Republic of)
  • Ham, Youngrok, Chungnam National University, Daejeon, Korea (the Republic of)
  • Na, Ki Ryang, Chungnam National University, Daejeon, Korea (the Republic of)
  • Lee, Kang Wook, Chungnam National University, Daejeon, Korea (the Republic of)
  • Choi, Wonjung, Chungnam National University, Daejeon, Korea (the Republic of)
  • Chang, Yoon-Kyung, The Catholic University of Korea, Daejeon, Korea (the Republic of)
Background

Reactive oxygen species (ROS) are thought to be a major factor in the development of acute renal injury and renal fibrosis in unilateral ureteral obstruction (UUO). NAD(P)H:quinone oxidoreductase 1 (NQO1) is a well-known antioxidant protein that regulates ROS generation. We generate the NQO1 donor, KL1333 and investigate whether KL1333 modulates the renal injury in UUO mice.

Methods

in vivo, 10 weeks old C57BL/6 male mice were divided 4 groups as following, sham, sham with KL1333, UUO, UUO with KL1333. KL1333 was treated oral route, 10mg/kg, daily. UUO were generated by tying left ureter, and after 7 days, the mice were sacrificed and kidney tissue were collected. in vitro, TGF beta treated HK2 cell were used. We analyzed renal injury using various stains, oxidative stress and tubular apoptosis using western blot and immunohistochemical stains.

Results

UUO mice kidney showed increased alpha SMA, collagen, masson trichrome stained area, and renal inflammation, compared to sham kidney. the KL1333 treatment decreased alpha SMA, collagen, masson trichrome stained area, and renal inflammation in UUO mice kidney. In addition, KL1333 increased the levels of HO-1, catalase, UCP2 in UUO mice kidney. Also, KL1333 increased NQO1, p-sirt1, and NAD+/NADH ratios in UUO mice. These finding indicate that KL1333 decreased UOO-induced oxidative stress and renal fibrosis.

Conclusion

NQO1 activation using KL1333 might be beneficial for ameliorating renal injury induced by UUO mice.