Quercitrin protects against oxidative stress-induced injury in lung fibroblast cells via up-regulation of Bcl-xL

The cytoprotective effect of quercitrin (QR) against oxidative stress induced cell damage by hydrogen peroxide (H2O2) in Chinese hamster lung fibroblast (V79-4) cells was investigated. QR evidenced a scavenging effect of 1,1-diphenyl-2-picrylhydrazyl (DPPH), superoxide, hydroxyl radicals and on intracellular ROS, and thus prevented lipid peroxidation. As a result, QR reduced H2O2-induced cell death and apoptosis in V79-4 cells. Moreover, H2O2 induced the cleavage of caspase-3, -9, and poly-ADP-ribose polymerase (PARP) and a reduction in Bcl-xL levels, whereas pretreatment with QR significantly inhibited caspase-3, -9, and PARP cleavage and the reduction in Bcl-xL levels, and ultimately ameliorated H2O2-induced apoptosis. Taken together, these results indicate that the treatment of V79-4 cells with QR can block H2O2-induced apoptosis via the regulation of Bcl-xL. QR may be exploited as a biopreservative in food applications or as a health supplement to alleviate oxidative stress.

► We have investigated the cytoprotective effects of QR against H2O2-induced cell damage.
► QR evidenced a scavenging effect of free radicals and on intracellular ROS.
► As a result, QR reduced H2O2-induced cell death and apoptosis in V79-4 cells.
► QR-induced cytoprotective effects were mediated through Bcl-xL pathway.