Protective Effects of Safflor Yellow A Against H2O2-induced Oxidative Stress Injury in PC12 Cells via Nrf2/HO-1 Pathway

Abstract

Background Safflor yellow (SY) is a water-capacitive component of dried flowers, mainly from safflor in the safflower family, which contains a large amount of bruthin A, or Safflor yellow A (SYA) for short. Studies have reported the protective effects of SYA against oxidative stress injury in nerve cells. Materials and Methods In this study, H 2 O 2 -treated PC12 cells were used as experimental materials to explore how SYA plays a protective role against nerve cells after oxidative stress and to analyze the molecular mechanism of SYA. PC12 cells were treated with H 2 O 2 and SYA solution. Cell proliferation is then detected with Cell Counting Kit-8 (CCK-8). The detection method is 5-(and 6)-chloromethyl-2′,7′-dichloro-dihydrofluorescein diacetate (CM-H2DCF-DA) staining reactive oxygen species (ROS). Levels of apoptosis-related proteins, including Bcl2-associated X protein (Bax), B-cell lymphoma (Bcl-2), caspase-3, and cleaved caspase-3, and oxidative stress regulators, namely, nuclear factor erythroid-2-related actor 2 (Nrf2) and heme oxygenase 1 (HO-1), were detected by western blotting. Results The CCK-8 assay results showed that the survival rate of H 2 O 2 -induced PC12 cells was significantly increased after SYA treatment. Fluorescence microscopy (CM-H2DCF-DA staining) indicated that SYA decreased H 2 O 2 -induced apoptosis in PC12 cells by reducing intracellular ROS. Western blotting analysis showed that SYA upregulated the expression of Nrf2, HO-1, and Bcl-2 and downregulated the expression of Bax, caspase 3, and cleaved caspase-3 in H 2 O 2 -induced PC12 cells. Conclusion SYA does protect the nerve cells from oxidative stress damage. Its mechanism of action is mainly related to whether the Nrf2/HO-1 pathway is activated.