Torularhodin Ameliorates Oxidative Activity in Vitro and D-Galactose-Induced Liver Injury via the Nrf2/HO-1 Signaling Pathway in Vivo

摘要

Torularhodin is a natural product extracted from Sporidiobolus pararoseus and has a similar chemical structure to beta-carotene. The antioxidative effects of torularhodin were investigated using DPPH, ABTS, a cell oxidative damage model in vitro, and a D-galactose-induced liver-injured mouse model in vivo. Cell experiments demonstrated that torularhodin had a powerful effect on oxidative damage caused by H2O2 to AML12 cells. Torularhodin significantly reduced inflammatory cytokines and increased the activity of antioxidant enzymes both in mouse serum and the liver. The inhibition of D-galactose-induced oxidative damage in the liver was correlated with the torularhodin-mediated effects on improving the activity of Nrf2/ HO-1, reducing the expression of Bax and NF-kappa B p65 by western blot analysis. RT-PCR results demonstrated torularhodin upregulated the antioxidative mRNA expression of Nrf2, NQO1, and HO-1 in the liver. In summary, torularhodin significantly scavenged free radicals and prevented oxidative damage in vitro and reduced D-galactose-induced liver oxidation via promotion of the Nrf2/HO-1 pathways in vivo.