Comparative Effects of Schisandrin A, B, and C on Acne-Related Inflammation

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 mu M 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 mu M, while schisandrin A required a concentration of 10 mu M 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-kappa B. 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.