Benzo[a]pyrene (BaP), a ubiquitous environmental pollutant, is formed by incomplete combustion of organic materials, and causes oxidative damage to cells and tissues due to reactive oxygen species (ROS). The purpose of this study is to investigate the inhibition of Tanshinone IIA and Baicalin on the formation of BaP as well as the cytotoxicity in human umbilical vein endothelial cells (HUVECs) induced by BaP. The results showed that BaP formations in mainstream smoke were inhibited by 21μg/cigarette of Tanshinone IIA with a 12.8% decrease, and by 60μg/cigarette of Baicalin with an 11.1% decrease, respectively. Tanshinone IIA could protect HUVECs from the damage caused by BaP in a dose-dependent manner from 7.5 to 30μg/ml. 6μg/ml Baicalin significantly increased the cell survival rate from 47.37% to 84.21% compared with BaP-treated cells. Both Tanshinone IIA and Baicalin markedly attenuated the increase of LDH release, enhanced the activity of SOD and GPx and inhibited the generation of MDA in BaP-damaged HUVECs in vitro. In vivo exploration showed that the two compounds were capable of enhancing the activity of SOD and inhibiting generation of MDA in mainstream smoke-damaged in mice. Superoxide anion radical and hydroxyl radical were obviously inhibited by Tanshinone IIA and Baicalin. These data demonstrate an inhibition of Tanshinone IIA and Baicalin on the formation of BaP and the cytotoxicity on HUVECs related to free Radical induced by BaP.
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