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The benefitial role of Ginsenoside Rg3 (Rg3) have been demonstrated through different mechanisms. However, the specific evaluation of its renal-protective effect and the involvement of autophagy remain unclear. This study aims to examine how Rg3 induces autophagy flux and diminishes renal cell death in renal ischemia reperfusion injury (IRI).
C57Bl/6 mice were categorized into the subsequent groups: sham; sham treated with Rg3; IRI mice treated with saline; IRI mice treated with Rg3. Kidneys and blood samples were obtained 24 hours after the surgical procedure (sham and IR operation). Renal function, kidney histology, and the protein expression of autophagy markers were assessed.
In the IRI mice group, there was an elevation of BUN and s-Cr levels compared to the sham group. However, the administration of Rg3 resulted in a reduction of BUN and s-Cr levels in the IRI mice. Furthermore, Rg3 treatment led to a decrease in renal injury, as evidenced by a lower renal tubular cell detachment and necrosis score in the IRI mice. The Rg3-treated IRI mice exhibited reduced oxidative stress and improved autophagy, characterized by increased levels of LC3 and Beclin-1, decreased levels of p62, and higher levels of renal ATP6E compared to the IRI mice treated with saline. Additionally, Rg3 treatment promoted the phosphorylation of AMPK in the kidneys of IRI mice.
Ginsenoside Rg3 (Rg3) induces activation AMPK-induced-autophagy flux and diminishes renal cell death in acute renal renal injury via ischemia reperfusion.