Betulinic acid protects against renal damage by attenuation of oxidative stress and inflammation via Nrf2 signaling pathway in T-2 toxin-induced mice.

Betulinic acid (BA) is a pentacyclic triterpenoid compound with potential antioxidant and anti-inflammatory effects. In this study, T-2 toxin was injected intraperitoneally in mice to establish kidney damage model and to evaluate the protective effects of BA and further reveal the molecular mechanism. BA pretreatment inhibited the T-2 toxin-stimulated increase in serum Crea, but showed no significant effect on serum Urea. BA pretreatment alleviated excessive glomerular hemorrhage and inflammatory cell infiltration in kidneys caused by T-2 toxin. Moreover, pretreatment with BA mitigated T-2 toxin-induced renal oxidative damage by up-regulating the activities of SOD and CAT, and the content of GSH, while down-regulating the accumulation of ROS and MDA. Meanwhile, BA pretreatment markedly attenuated T-2 toxin-induced renal inflammatory response by decreasing the mRNA expression of IL-1β, TNF-α and IL-10, and increasing IL-6 mRNA expression. Furthermore, mechanism research found that pretreatment with BA could activate Nrf2 signaling pathway. It was suggested that BA ameliorated the oxidative stress and inflammatory response of T-2 toxin-triggered renal damage by activating the Nrf2 signaling pathway.