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Abstract: PO0370

Ginsenoside Rg3 Attenuates Ischemia Reperfusion-Induced Renal Injury in Mice via Induction of Autophagy Flux

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Shin, Jin Ah, Chungnam National University School of Medicine, Daejeon, Daejeon, Korea (the Republic of)
  • Choi, Dae Eun, Chungnam National University School of Medicine, Daejeon, Daejeon, Korea (the Republic of)
  • Jeong, Jin young, Chungnam National University School of Medicine, Daejeon, Daejeon, Korea (the Republic of)
  • Hwang, Haet Bit, Chungnam National University School of Medicine, Daejeon, Daejeon, Korea (the Republic of)
  • Han, Soo hyun, Chungnam National University School of Medicine, Daejeon, Daejeon, Korea (the Republic of)
  • Lee, Eu Jin, Chungnam National University School of Medicine, Daejeon, Daejeon, Korea (the Republic of)
  • Ham, Youngrok, Chungnam National University School of Medicine, Daejeon, Daejeon, Korea (the Republic of)
  • Na, Kiryang, Chungnam National University School of Medicine, Daejeon, Daejeon, Korea (the Republic of)
  • Lee, Kang Wook, Chungnam National University School of Medicine, Daejeon, Daejeon, Korea (the Republic of)
Background

Ginsenoside Rg3 (Rg3) has been shown as protective effects via various mechanism. However, the reno-protective effect and the role of autophagy are not clearly evaluated. This study investigate Rg3 induces autophagy flux and reduces renal cell death in renal ischemia reperfusion injury (IRI).

Methods

C57Bl/6 mice were divided into the following groups: sham; Rg3 treated sham; saline treated IRI mice; Rg3 treated IRI mice. Kidneys and blood were collected 24h after operation of mice (sham and IR operation). Renal function, kidney histology, and the protein expression of autophagy signals were evaluated.

Results

In IRI mice, the levels of BUN and s-Cr were increased, compared to sham. The Rg3 treatment decreased the BUN and s-Cr in IRI mice. In addition, Rg3 treatment decreased the renal injury score including the renal tubular cell detachment and necrosis in IRI mice. Rg3 treated IRI mice showed significantly less oxidative stress and autophagy impairment, greater amounts of LC3 and Beclin-1, lower amounts of p62, and higher levels of renal ATP6E compared to saline treated IRI mice. Rg3 treatment also increased phosphorylation of AMPK in IRI mice kidney.

Conclusion

Rg3 has renoprotection against renal IR injury via enhancement of autophagy flux.