Triptolide suppresses ultraviolet B-enhanced sebum production by inhibiting the biosynthesis of triacylglycerol in hamster sebaceous glands in vivo and in vitro.

Ultraviolet B (UVB) irradiation causes alterations in cutaneous barrier function, including excessive production of sebum in sebaceous glands, which is associated with the aggravation of acne. This study aimed to evaluate the inhibitory effects of triptolide, a diterpenoid triepoxide from Tripterygium wilfordii Hook F, on sebocytic lipogenesis in UVB-irradiated hamster skin in vivo and in vitro. Topical application of triptolide decreased the UVB-enhanced sebum accumulation in the sebaceous glands of hamster skin. The level of triacylglycerol (TG), a major sebum component, on the skin surface was reduced by triptolide treatment in UVB-irradiated hamsters, whereas there was no change in that of free-fatty acids and cholesterol, which are minor sebum components. UVB irradiation significantly enhanced TG production (P<0.01 in extracellular lipids, P<0.05 in intracellular lipids), and the activity of acyl coenzyme A/diacylglycerol acyltransferase (DGAT), a rate-limiting enzyme of TG synthesis, in differentiated hamster sebocytes (P<0.05 at 6 h and UVB of 0.62 kJ/m2, P<0.001 at 24 h and UVB 0.37 or 0.62 kJ/m2). Furthermore, triptolide significantly inhibited UVB-enhanced TG production (P<0.05 at 28 nM and P<0.01 at 56 and 112 nM triptolide) and DGAT activity (P<0.01 at 28 nM and P<0.001 at 56 and 112 nM triptolide) in differentiated hamster sebocytes. These results provide novel evidence that triptolide decreases UVB-enhanced sebum production by inhibiting DGAT-dependent TG biosynthesis in differentiated hamster sebocytes. These findings may be applicable to the prevention of acne aggravation.