Antioxidants Inhibit Subsequent Lipid Production via Sebaceous Gland Cell Differentiation

The sebaceous gland is composed of sebaceous gland cells that accumulate intracellular lipid droplets when undergoing differentiation. The extent of lipid droplet formation within the sebaceous gland cells thus represents their differentiation status. On reaching maturity, the sebaceous gland cells are then destroyed and the intracellular lipids are secreted to the skin surface whereby they form a weakly acidic sebum film with intercellular lipids of the stratum corneum and sweat. The main sebum lipid is composed of triglycerides, including cholesterol, free fatty acids and other members. Sebum prevents invasion of foreign matter from the outside and protects the skin from irritation of various substances. It also has a moisture retention function and sterilization action. In atopic dermatitis patients, the amount of sebum decreases, which is thought to be caused by decreased sebum production and/or secretion. Excessive secretion of sebum is associated with skin diseases such as acne and lipid peroxide production [1]. In addition, secretion of sebum is promoted not only by environmental factors such as ultraviolet (UV) rays (predominantly UVB) and temperature rise, but also by external factors such as gamma oryzanol, herbal extracts (liquorice, carrot, yokuinin), and endogenous factors such as androgen hormones [2,3]. Furthermore, lipid peroxide, which is also increased by UV rays (UVB) and secreted to the skin surface, irradiated UV rays (UVB), and lipid peroxides destroy the skin barrier function. Testosterone, an androgenic hormone, is converted to dihydrotestosterone by 5-reductase, which stimulates the sebaceous glands and increases sebum secretion. Furthermore, these components increase the sebaceous gland size [4-6], cell division [7], and sebum production [8,9]. Interestingly, secretion of sebum is promoted by UV rays (UVB) and male hormones [10,11] butis suppressed by pyridoxine or retinoic acid.