Protective effects of Scutellaria baicalensis Georgi against hydrogen peroxide-induced DNA damage and apoptosis in HaCaT human skin keratinocytes.

Oxidative stress due to excessive accumulation of reactive oxygen species (ROS) is one of the risk factors for the development of several chronic diseases. In this study, we investigated the protective effects of rhizome ethanol extract (SBRE) against oxidative stress-induced cellular damage and elucidated the underlying mechanisms in the HaCaT human skin keratinocyte cell line. Our results revealed that treatment with SBRE prior to hydrogen peroxide (HO) exposure significantly increased viability of HaCaT cells. SBRE also effectively attenuated HO-induced comet tail formation and inhibited the HO-induced phosphorylation levels of the histone γH2AX, as well as the number of apoptotic bodies and Annexin V-positive cells. In addition, SBRE exhibited scavenging activity against intracellular ROS generation and restored the mitochondrial membrane potential loss by HO. Moreover, HO enhanced the cleavage of caspase-3 and degradation of poly (ADP-ribose)-polymerase, a typical substrate protein of activated caspase-3, as well as DNA fragmentation; however, these events were almost totally reversed by pretreatment with SBRE. Furthermore, SBRE increased the levels of heme oxygenase-1 (HO-1), which is a potent antioxidant enzyme, associated with the induction of nuclear factor-erythroid 2-related factor 2 (Nrf2). According to our data, SBRE is able to protect HaCaT cells from HO-induced DNA damage and apoptosis through blocking cellular damage related to oxidative stress through a mechanism that would affect ROS elimination and activating the Nrf2/HO-1 signaling pathway.