Esculentoside A inhibits LPS-induced acute kidney injury by activating PPAR-γ

- EsA attenuated LPS-induced kidney histological change, as well as BUN and creatinine levels.
- EsA also inhibited LPS-induced TNF-α, IL-1β, and IL-6 production.
- LPS-induced NF-κB activation was significantly suppressed by treatment of EsA.
- EsA up-regulated the expression of PPAR-γ in a dose-dependent manner.

Acute kidney injury (AKI) is a major clinical problem associated with high morbidity and mortality. Esculentoside A (EsA), a kind of saponin isolated from the root of the Chinese herb Phytolaca esculenta, has been reported to have anti-inflammatory effect. In this study, we aimed to investigate the protective effects of EsA on LPS-induced AKI in mice. The protective effects of EsA was evaluated by detecting kidney histological change, blood urea nitrogen (BUN) and creatinine levels, and inflammatory cytokines production. The results showed that EsA significantly attenuated LPS-induced kidney histological change, as well as BUN and creatinine levels. EsA also inhibited LPS-induced TNF-α, IL-1β, and IL-6 production. LPS-induced NF-κB activation was significantly suppressed by treatment of EsA. In addition, EsA up-regulated the expression of PPAR-γ in a dose-dependent manner. In conclusion, EsA protected mice effectively from LPS-induced AKI by PPAR-γ, which subsequently inhibited LPS-induced inflammatory response.