Kidney Week

Abstract: TH-PO617

Indoxyl Sulfate-Induced Apoptosis in C2C12 Cells

Session Information

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

Category: Health Maintenance, Nutrition, and Metabolism

• 1300 Health Maintenance, Nutrition, and Metabolism

Authors

• Kang, Seok hui, Yeungnam University Hospital, Daegu, Korea (the Republic of)

Seok hui Kang,

• LEE, YOUNSU, Yeungnam University Medical Center, Deagu, Korea (the Republic of)

YOUNSU LEE,

• Do, Jun-Young, Yeungnam University Hospital, Daegu, Korea (the Republic of)

Jun-Young Do,

Background

Indoxyl sulfate is a well-known uremic toxin and associated with skeletal muscle atropy in chronic kidney disease. However, there are few studies regarding precise molecular mechanism. The aim of the study was to identify indoxyl sulfate induced apoptosis as a molecular mechanism.

Methods

Mouse C₂C₁₂ myoblast were purchased and cultured in Dulbecco’s modified eagle medium. After cell adhesion, cultured medium was changed containing with uremic toxins and cultured. Reactive oxygen species (ROS) production and CCK assays were performed. Tunnel staining, phase contrast microscopy, and flowcytometry were also performed.

Results

ROS production was increased as dose of indoxyl sulfate increased. Apoptosis was increased as dose of indoxyl sulfate increased. In addition, tunnel stained cell count increased as dose of indoxyl sulfate. Cell confluence decreased as dose of indoxyl sulfate. Flowcytometry using Annexin V and PI showed that proportion of double positive cell increased as dose of indoxyl sulfate.

Conclusion

Our results demonstrate that indoxyl sulfate is associated with apoptosis of myoblast through ROS production.