Schizandrin B is extracted from Schisandra chinensis (Turcz.) Baill. This study evaluated the photoprotective effect of Schizandrin B on oxidative stress injury of the skin caused by UVB-irradiation and the molecular mechanism of the photoprotective effect of Schizandrin B, and we firstly found that Schizandrin B could block Cox-2, IL-6 and IL-18 signal pathway to protect damage of skin cells given by UVB-irradiation. In the research, we found that Schizandrin B can attenuate the UVB-induced toxicity on keratinocytes and dermal fibroblasts in human body, and can outstandingly eliminated intracellular ROS produced by UVB-irradiation. These results demonstrate that Schizandrin B can regulate the function of decreasing intracellular SOD's activity and increasing the expression level of MDA in HaCaT cells result from the guidance of UVB, and it markedly reduced the production of inflammatory factors such as Cox-2, IL-6 or IL-18, decreased the expression level of MMP-1, and interdicted degradation process of collagens in UVB-radiated cells. Therefore, skin keratinocytes can be effectively protected from UVB-radiated damage by Schizandrin B, and UVB-irradiation caused inflammatory responses can be inhibited by attenuating process of ROS generating.

Inflammatory responses induced by Propionibacterium acnes are a major etiological factor in the pathogenesis of acne vulgaris. Schisandrin A, schisandrin B, and schisandrin C are the representative lignans of Schisandra chinensis (Turcz.) Baill. extract. Although anti-inflammatory effects of the lignans have been shown, their effects on acne-related inflammation caused by P. acnes have not been investigated and compared. We pretreated THP-1 human monocytic cells with 5, 10, and 20 μM schisandrin A, B, and C, and stimulated the cells with P. acnes. Schisandrin B and C inhibited the release of inflammatory cytokines at a concentration of 5 μM, while schisandrin A required a concentration of 10 μM to exert the effects. All of the schisandrins decreased the levels of toll-like receptor 2, and schisandrin B and C reduced the intracellular mRNA expression of the receptor gene. We also studied the influence of schisandrins on the MAPK signaling pathway. Schisandrin A suppressed the P. acnes-induced activation of JNK, while exerting only a weak effect on ERK and p38. Schisandrin B exerted a strong effect on p38, a lesser effect on ERK, and almost no effect on JNK. Schisandrin C inhibited the phosphorylation of all three proteins, especially ERK. Furthermore, the three lignans also prevented the nuclear translocation of NF-κB. These results contribute to our understanding of the mechanisms underlying the effects of the three lignans on P. acnes-induced inflammation and suggest that schisandrins might be developed as pharmacological agents for acne therapy.