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

脂肪生成 脂滴 自噬 溶酶体 尼罗河红 油酸 油红O PI3K/AKT/mTOR通路 化学 生物化学 细胞生物学 亚油酸 自噬体 脂质代谢 脂肪酸 生物 细胞凋亡 体外 脂肪生成 物理 量子力学 荧光
作者
Kaibo Wan,Jian Li,Nyuk Ling,Timson Chen,Chen Ya,Zhizhen Li,Christos C. Zouboulis,Guangli Wang,Jing Wang
出处
期刊:International Journal of Cosmetic Science [Wiley]
标识
DOI:10.1111/ics.13047
摘要

Abstract 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.

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