Kirenol Inhibits B[a]P-Induced Oxidative Stress and Apoptosis in Endothelial Cells via Modulation of the Nrf2 Signaling Pathway

Figure 2

KRL inhibits ROS formation. HUVECs cells confluent at 80% were incubated with B[a]P (5 μmol) and/or KRL 10 and 25 μmol for 60 minutes. (a) DCFH2-DA was made use for the purpose of measuring generation of intracellular ROS. After reacting with ROS, DCFH2-DA metabolized into DCF, which, in turn, was proportionate to ROS’s generation. (b) KRL effect on NO production in B[a]P-induced oxidative stress. (c) KRL on oxidative marker 4-HNE protein activation. Data was represented as the of triplicate values (), and represents a significant discrepancy when compared to the control group. On the other hand, ^# signifies major differences compared to the B[a]P alone and KRL with the B[a]P treatment groups.

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