Camellia saponin modulates oleic acid/linoleic acid-induced lipogenesis in human sebocytes through lipophagy activation.

Background: Oily skin not only threatens people with aesthetic and hygienic discomfort but also confronts them with annoying skin problems. To explore new skin care ingredients from herbal or plant extracts and understand their underlying mechanism for sebum control would assist in the discovery of desirable sebosuppressive agents, though it is still a deserving and challenging task.

Aim: To explore the effect of Camellia saponin (CS) on modulating the lipogenesis of human sebocytes. Moreover, to explore the underlying mechanism of CS on oleic acid/linoleic acid (OL) mixture stimulated lipid accumulation.

Methods: The lipid accumulation model of cells was constructed by OL-induction in vitro. The lipid synthesis in SZ95 sebocytes was detected by Oil Red O, Nile Red and BODIPY staining and the distribution of lipid droplets and autophagosomes were evaluated by transmission electron microscopy (TEM). Fluorescence staining, immunofluorescence and western blot (WB) were used to characterize the spatial localization of lipid droplets (LDs)/autophagosome/lysosome, the levels of LC3 and P62 proteins related to intracellular autophagy, as well as the pH of lysosome.

Results: CS treatment significantly relieved OL-induced lipid accumulation in SZ95 sebocytes. Furthermore, CS maintained lysosomal acid environment to promote the fusion of autophagosome and lysosome, thus recovering the OL-induced blockage of autophagy flow. We also found that CS activated AMPK, and down-regulated mTOR in SZ95 sebocytes.

Conclusion: CS was able to relieve OL-stimulated sebum accumulation in cultured human SZ95 sebocytes through lipophagy, in which process CS maintained lysosomal acid environment and activated the AMPK/mTOR pathway.