Z‐ligustilide ameliorated ultraviolet B ‐induced oxidative stress and inflammatory cytokine production in human keratinocytes through upregulation of N rf2/ HO ‐1 and suppression of NF ‐ κ B pathway

Ultraviolet B ( UVB ), a harmful environmental factor, is responsible for a variety of skin disorders including skin inflammation through reactive oxygen species ( ROS ) and inflammatory mediator production. Here, we investigated the effect of Z‐ligustilide (Z‐lig), an active ingredient isolated from the medicinal plants Cnidium officinale and Angelica acutiloba , on UVB ‐induced ROS generation and inflammatory mediator production in normal human epidermal keratinocytes ( NHEK s) as well as its underlying mechanisms. Z‐lig significantly rescued UVB ‐induced NHEK s damage in a dosage‐dependent manner. Pretreatment of NHEK s with Z‐lig inhibited UVB ‐induced ROS production in NHEK s. Both silencing the nuclear factor E2‐related factor 2 (Nrf2) and the supplement of tin protoporphyrin IX (Sn PP ), a haeme oxygenase‐1 ( HO ‐1) inhibitor, cancelled the inhibitory effect of Z‐lig on UVB ‐induced ROS upregulation in NHEK s. Moreover, pretreatment of NHEK s with Z‐lig reduced UVB ‐induced nuclear factor kappa B ( NF ‐ κ B)‐dependent inflammatory mediators ( IL ‐6, IL ‐8 and MCP ‐1) production at both m RNA and protein level. In the presence of Z‐lig, UVB ‐induced NF ‐ κ B subunit p65 nuclear translocation was abolished, and the I κ B α degradation was suppressed. Taken together, these findings suggest that Z‐lig can suppress UVB ‐induced ROS generation through Nrf2/ HO ‐1 upregulation and inflammation by suppressing the NF ‐ κ B pathway, suggesting that Z‐lig may be beneficial in protecting skin from UVB exposure.