Schisandrin B protects human keratinocyte-derived HaCaTcells from tert-butyl hydroperoxide-induced oxidative damage through activating the Nrf2 signaling pathway.

Abstract

Schisandrin B (Sch B), an active extract of Schisandrachinensis, has demonstrated antioxidant activity in a number of invitro and invivo models. In the present study, the capacity of Sch B to protect against oxidative injury in keratinocytes using the human keratinocyte‑derived HaCaT cell line was investigated. To induce oxidative injury, tert‑Butyl hydroperoxide (tBHP) was employed. The results indicate that Sch B efficiently reduced tBHP‑induced cell death, reactive oxygen species (ROS) generation, protein oxidation, lipid peroxidation and DNA damage. Sch B also effectively attenuated the loss of mitochondrial membrane potential (MMP), and restored adenosine triphosphate (ATP) levels in tBHP‑injured HaCaT cells. Furthermore, Sch B enhanced the expression of key antioxidant enzymes, including catalase, heme oxygenase‑1, glutathione peroxidase, and superoxide dismutase, and further engaged the nuclear factor‑erythroid 2‑related factor 2 (Nrf2) signaling pathway by modulating its phosphorylation through activating multiple upstream kinases, including protein kinase B, adenosine monophosphate‑activated protein kinase and mitogen‑activated protein kinases (MAPKs). The present study suggests that Sch B provides a protective effect in keratinocytes in response to oxidative injury via reinforcing the endogenous antioxidant defense system. Therefore, it may be applied as an adjuvant therapy or in health foods to delay the skin aging process and the onset of skin diseases caused by oxidative stress.