Abstract
Background: Acne vulgaris is characterized by the enhancement of sebaceous lipogenesis and sebum secretion, and apart from retinoids and some natural products there are few effective antiacne agents that directly suppress sebum production and accumulation in sebaceous glands. Objective: We examined the effects of β-cryptoxanthin (β-CRX), which is a carotenoid pigment most abundant in Citrus unshiu Marcovich (Satsuma mandarin orange) and plays a role as a vitamin A precursor on sebum production and accumulation in hamster sebaceous gland cells (sebocytes). Materials and methods: The regulation of sebum production was examined by the measurement of triacylglycerols (TGs), the major sebum component, and oil red O staining in insulindifferentiated hamster sebocytes. The expression of diacylglycerol acyltransferase-1 (DGAT-1), a rate-limiting enzyme of TG biosynthesis, and perilipin 1 (PLIN1), a lipid storage droplet protein, was analyzed using real-time PCR and Western blotting. Results: Hamster sebocytes constitutively produced TGs during cultivation and the production of TGs was enhanced by insulin treatment. Both constitutive and insulin-enhanced TG productions were dose- and time-dependently inhibited by β-CRX as well as 13-cis retinoic acid. In addition, the gene expression of DGAT-1 was suppressed by β-CRX in the sebocytes. Furthermore, the insulin-en- hanced sebum accumulation as lipid droplets was reduced in the β-CRX-treated cells. Moreover, β-CRX was found to suppress the gene expression and production of PLIN1 in insulin-differentiated hamster sebocytes. Conclusions: These results provide novel evidence that β-CRX is an effective candidate for acne therapy by its ability to exert dual inhibitory actions against DGAT-1-dependent TG production and PLIN1-mediated lipiddroplet formation in hamster sebocytes.
Highlights
The pathogenesis of acne, a common inflammatory skin disease [1,2], is characterized by: 1) excess sebum production in sebaceous glands; 2) the formation of microcomedones, which is closely associated with the hyperkeratinization of the follicular wall and infundibulum; 3) the hyperproliferation of Propionibacterium acnes (P. acnes); and 4) the induction of inflammatory reactions such as the acceleration of cytokine production and the biosynthesis of arachidonic acid metabolites in keratinocytes, sebocytes, and invaded inflammatory cells [3,4]
We demonstrated that β-CRX suppresses the production of TGs and the gene expression of diacylglycerol acyltransferase-1 (DGAT-1) in differentiated hamster sebocytes
Our previous study showed that the decrease of TG production by both 13-cisRA and atRA is closely related to that of DGAT activity as well as the DGAT-1 transcript in differentiated hamster sebocytes [18]
Summary
The pathogenesis of acne, a common inflammatory skin disease [1,2], is characterized by: 1) excess sebum production in sebaceous glands; 2) the formation of microcomedones, which is closely associated with the hyperkeratinization of the follicular wall and infundibulum; 3) the hyperproliferation of Propionibacterium acnes (P. acnes); and 4) the induction of inflammatory reactions such as the acceleration of cytokine production and the biosynthesis of arachidonic acid metabolites in keratinocytes, sebocytes, and invaded inflammatory cells [3,4]. Objective: We examined the effects of β-cryptoxanthin (β-CRX), which is a carotenoid pigment most abundant in Citrus unshiu Marcovich (Satsuma mandarin orange) and plays a role as a Vitamin A precursor on sebum production and accumulation in hamster sebaceous gland cells (sebocytes). Results: Hamster sebocytes constitutively produced TGs during cultivation and the production of TGs was enhanced by insulin treatment. Both constitutive and insulin-enhanced TG productions were dose- and time-dependently inhibited by β-CRX as well as 13-cis retinoic acid. Β-CRX was found to suppress the gene expression and production of PLIN1 in insulin-differentiated hamster sebocytes. Conclusions: These results provide novel evidence that β-CRX is an effective candidate for acne therapy by its ability to exert dual inhibitory actions against DGAT-1-dependent TG production and PLIN1-mediated lipid-droplet formation in hamster sebocytes
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