Dry skin is very a common skin problem, which frequently results in a rough, scaly quality to the skin. It will further cause chronic itch. Dryness was obviously associated with eczematous or psoriatic skin, and maintaining adequate skin hydration in the skin requires effort from two aspects:

  • skin barrier function improvement, such as reinforcing cornified envelope and order intercellular lamellar lipids to reduce trans‐epidermal water loss(TWEL), or increasing the content of natural moisturizing factors (NMF) in corneocytes.
  • intrinsic hydration capacity enhancement, such as increasing the content of endogenous glycerol, which served as a natural moisturizer, and HA in the skin. Aquaporins (AQP3) are abundantly expressed in the epidermis, and served as a channel to transport glycerol and water; hyaluronan synthetases 2 (HAS2) are also expressed by keratinocyte and located in the epidermis, which is responsible for the synthesis of large molecules of HA. Meanwhile, endogenous glycerol and HA play a vital role in skin hydration. It was proved that 10 μg/mL SBT seed oil treatment significantly increased expressions of AQP3 and HAS2 in comparison with negative control.

AQP3, as an aquaglyceroporin, can transport water, glycerol, and urea, which has a function in keratinocyte proliferation and differentiation. Mature epidermis develops based on the balance of cell proliferation and differentiation; therefore, AQP3 was closely associated with wound healing, disrupted skin barrier recovery, and stratum corneum hydration. AQP3 plays a pivotal role in water and glycerol transport. Over-expression of AQP3 causes more water to be transported from the dermis to the epidermis to maintain skin hydration. Previous studies indicated that all‐trans retinoic acid treatment up‐regulates AQP3 expression, which is accompanied by a rise in water movement. AQP3 absence delayed skin barrier recovery and wound healing.

AQP3 is abundantly expressed and localized to the basal layer containing proliferating keratinocytes and a spinous layer containing early differentiated keratinocytes, suggesting that AQP3 might involve in cell proliferation and early differentiation. It has been suggested that AQP3 evidently promoted cell proliferation through glycerol transport because glycerol served as a crucial regulator of cellular ATP energy.

Previous studies have shown that re‐expression of AQP3 in AQP3‐deficient cells enhanced expression of early differentiating marker K10 (keratin 10) and K1 (keratin 1), as well as terminally differentiated marker LOR (loricrin), and urea transported by AQP3 also has been proved that induced different early differentiating markers expressions.

Nevertheless, the role of AQP3 in cell proliferation and differentiation was associated with various skin diseases. Studies suggested that AQP3 expression level was decreased in lesional and peri‐lesional psoriasis skin compared with healthy control, which was accompanied by a decline in skin hydration and a rise of TEWL (trans‐epidermal water loss).

Other studies further suggested that psoriasis is a Th1 cytokine‐dominant skin disease with over-expression of Th1 cytokine‐TNF (tumor necrosis factor)‐α and TNF receptor‐1, which inhibited AQP3 expression. An evident decrease in AQP3 expression was observed in keratinocytes derived from vitiligo lesions, and down‐regulation of AQP3 reduced the downstream signaling including PI3K and E‐cadherin, which were associated with keratinocyte survival, and further led to the loss of cell‐cell adhesion and decline of keratinocyte‐derived growth factors, and finally cause the death of adjacent melanocytes. The above results collectively suggested that AQP3 might use as a therapeutic target for dry skin, psoriasis, and vitiligo.

HA, a large glycosaminoglycan mainly exists in ECM and can absorb water more than 1,000 times its weight, which is critical for skin hydration. According to reports, HAS2 can synthesize HA. It has been previously reported that UV exposure induced loss of HA and inhibition of HAS in the skin. HA was involved in the natural responses of epidermal in wound‐healed and barrier recovery in AD, including proliferation and migration of keratinocytes. It has been shown that HA bound to its best‐characterized cell surface receptor, CD44, induced LB (lamellar body) formation and secretion, and enhanced expressions of keratinocyte differentiation markers including K10, profilaggrin, which was very important to skin barrier repair and maintaining skin hydration.

Sea buckthorn seed oil contains high amounts of PUFA, such as oleic acid (OA), linoleic acid (LA), and α‐linolenic acid (ALA). LA is the richest fatty acid in the epidermis and is the precursor to synthesizing ceramide, which is a predominant substance responsible for the skin permeability barrier. LA was generally acknowledged as an inflammation suppressor, which could be used for the treatment of inflammation‐related skin diseases, such as AD. It has been found that LA attenuated pigmentation through anti‐inflammation and reduced tyrosinase activity. Moreover, LA inhibits the growth of Staphylococcus aureus by influencing the synthesis of proteins and nucleic acids.

OA has been proved that it can inhibit tyrosinase activity, and it is also used to treat psoriasis. ALA and its derivative have been found that they may contribute to lamellar body formation, cytokine inhibition, lipoxygenase repression, SC differentiation, and maturation, which might relieve inflammatory‐related dermatoses including acne, AD, psoriasis, and lupus. Sea buckthorn seed oil containing abundant OA, LA, and ALA has been validated that had a positive effect on AD through suppression of inflammation and repaired lipid metabolism disorders induced by UV exposure.

In our study, it was proved that sea buckthorn seed oil can improve skin hydration through increasing AQP3 and HAS2 expressions, which indicates it is a promising natural compound to boost the skin’s ability to retain moisture.