ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

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: SA-PO605

Impact of Ciprofloxacin on Renal Tubular Epithelial Injury Through the Interaction of Autophagy and Apoptosis

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Park, Woo Yeong, Keimyung University School of Medicine, Daegu, Korea (the Republic of)
  • Park, Hayeon, Keimyung University School of Medicine, Daegu, Korea (the Republic of)
  • Jin, Kyubok, Keimyung University School of Medicine, Daegu, Korea (the Republic of)
  • Park, Sung Bae, Keimyung University School of Medicine, Daegu, Korea (the Republic of)
  • Han, Seungyeup, Keimyung University School of Medicine, Daegu, Korea (the Republic of)
Background

Autophagy and apoptosis play an important role in renal tubular epithelial injury by hypoxia, nutrient deprivation, and oxidative stress. Recent research reported that antibiotics might contribute to ischemic renal injury characterized by both apoptosis and inflammation, but the mechanism remains unclear. Therefore, we investigated the impact of ciprofloxacin on renal tubular epithelial injury through the interaction of autophagy and apoptosis.

Methods

We used MDCK cells, a model for renal distal tubular epithelial cells. We performed TUNEL assay to identify the effect of ciprofloxacin for cell viability under nutrient deprivation for 48 hours (hrs). We assessed apoptosis and autophagy markers to investigate the effect of ciprofloxacin through the interaction between apoptosis and autophagy.

Results

In the TUNEL assay, the ratio of apoptotic cells/total cells was significantly lower in the ciprofloxacin group (100 ug/mL) than in the control group (0 ug/mL) (7.17 ± 1.25 vs. 20.41 ± 1.04, P < 0.001). Among apoptosis markers, the ratio of pBax/Bax was reduced at 6 hr, and pBcl-2/Bcl-2 was increased at 12 hr in the ciprofloxacin group compared with the control group. In the MAPK pathway, located further upstream of Bax and Bcl-2, the ratio of pJNK/JNK, pp38/p38, and pERK/ERK was decreased at 12 hr in the ciprofloxacin group compared to the control group. The ratio of cleaved caspase 3/caspase 3, the final effector caspase, was decreased at 36 hr in the ciprofloxacin group compared with the control group. Among autophagy markers, the level of Beclin-1 was increased at 6 hr in the ciprofloxacin group compared with control group, and the level of LC3B was increased after 12 hr. Finally, activation of autophagy by ciprofloxacin during apoptosis by nutrient deprivation might cause recovery of renal tubular epithelial injury.

Conclusion

Ciprofloxacin can help to restore cell viability against renal tubular epithelial injury under nutrient deprivation condition, and the cell viability by ciprofloxacin might be associated with the crosstalk of autophagy and apoptosis. Therefore, ciprofloxacin is helpful to increase cell viability through activation of autophagy under ischemic renal injury.