To identify the possible mechanism of UV-induced superficial
SC barrier alterations, we investigated whether UVR disrupts
corneocyte cornified envelope (CE) maturation properties in
the same six subjects. Double staining with Nile red and antiinvolucrin
revealed no clear trend at day 1 (data not shown). By
day 14, UVR tended to stimulate CE maturation (increase in Nile
red) in UV only zone, while treatment with SPF or Moisturizer
alone or in combination tended to reduce response comparable
to control (Figure 4A and 4B). However due to the variation in
small sample size, no statistically significant difference was
detected.
DISCUSSION
Due to their benefits in promoting skin barrier strength and repair, incorporation of SC lipids into formulas has become increasingly popular across the skincare field.17 Since our skin is constantly exposed to UVR, it is crucial to delineate its influence on skin barrier, plus to assess the potential benefits of barrier-enforcing lipids formulations for solar protection. Here, we demonstrate the clinical efficacy of a ceramide-containing sunscreen and moisturizer routine in preventing UV-induced skin surface barrier changes.
Solar radiation leads to an immediate skin inflammatory response followed by a protective process, which clinically manifest as erythema and hyper-pigmentation respectively.18 We showed that treatment with ceramide-containing sunscreen alone or in combination with moisturizing cream prevented the initial erythema response, as well as reduced skin darkening at all timepoints compared to UV only and moisturizer alone (Figure 1A and 1B). The protective effects provided by the ceramide-containing sunscreen is likely due to its UV-filter capability, as the photoprotective clinical efficacy of sunscreens against UV-induced cutaneous responses are well documented.19 Although the exact mechanism awaits further investigation, growing evidence indicates that CERs also have anti-pigmentation properties.20 Future studies are needed to expand on these premises and determine the mechanisms of CERs depigmentation capabilities, and added benefits when combined with UV filters.
UV is shown to disrupt skin barrier integrity by increasing TEWL, decreasing skin hydration, promoting SC and epidermal thickness, plus changing skin lipids and proteins levels and structures.4,6,21 Despite the differences in study conditions, the variation of UVR effects on skin barrier-related endpoints remains poorly understood. Haratake et al, demonstrated that UVR (7.5 MED) can lead to a delayed impaired barrier response followed by rapid recovery, which was dependent on epidermal hyperproliferation and inflammation.22 Subsequently, Holleran et al, reported that the same UV dose after 24 hours caused incidence of damaged lamellar bodies (LBs) only at the stratum granulosum (SG) and SC interface, which contributed to the delayed in abnormal barrier permeability and no change in TEWL. Following 72 hours, he observed a deficient lamellar membrane in the lower SC and an increase in impaired LBs at SG/SC interface, causing elevated TEWL and compromised barrier. By 120 hours, there was a hyperproliferative response promoting thickening of the SG and arrival of normal lamellar membranes in the lower SC, which in turn resulted in the restoration of the epidermal barrier.23
In our study, UVR (2 MED) did not cause a drastic change in either TEWL nor hydration (Figure 2A and 2B), which could be attributed to the skin’s ability to delay barrier deficiency and rapidly recover from superficial damage. Nevertheless, treatment with ceramide-containing sunscreen in combination with moisturizer (SPF+Moisturizer) improved skin hydration over time, indicating that the skin water content, which is essential for maintaining barrier function, was both maintained and ameliorated. Moreover, we observed that UVR tended to alter skin surface organization patterns and promote corneocyte maturation (Figure 3 and 4). Out of the three corneocyte microstructural parameters evaluated, UVR significantly increased the appearance of weakly differentiated cells in untreated skin, which persisted up to day 14 and was prevented by treating with the sunscreen or moisturizer alone or in combination (Figure 3C and 3D). This phenomenon is consistent with the ability of UVR to decrease SC cohesion by altering intracellular lipids and corneodesmosomes to compromise barrier integrity.4 Altogether, our findings suggest that an increase in corneocyte maturation was a result of some degree of UV-induced skin barrier damage, disrupting superficial SC morphology. Thus, increased SC turnover or epidermal hyperplasia, as shown in prior studies, are all compensatory mechanisms that the skin barrier utilizes to adapt in response to UV stress to prevent subsequent damage.21–23 Our results indicate that a skincare routine combining a ceramide-containing sunscreen and moisturizer may prevent early UV-induced skin barrier damage and the consequent skin physiological alterations. However, some limitation should be noted. We were unable to compare the efficacy of our ceramidecontaining products with non-ceramide containing sunscreen and moisturizer due to limited test sites on subjects. Future studies will expand on our findings and determine the exact mechanism of CERs capabilities, plus added benefits when combined with UV filters and other ingredients for promoting skin barrier health in response to UV-induced stress.
Solar radiation leads to an immediate skin inflammatory response followed by a protective process, which clinically manifest as erythema and hyper-pigmentation respectively.18 We showed that treatment with ceramide-containing sunscreen alone or in combination with moisturizing cream prevented the initial erythema response, as well as reduced skin darkening at all timepoints compared to UV only and moisturizer alone (Figure 1A and 1B). The protective effects provided by the ceramide-containing sunscreen is likely due to its UV-filter capability, as the photoprotective clinical efficacy of sunscreens against UV-induced cutaneous responses are well documented.19 Although the exact mechanism awaits further investigation, growing evidence indicates that CERs also have anti-pigmentation properties.20 Future studies are needed to expand on these premises and determine the mechanisms of CERs depigmentation capabilities, and added benefits when combined with UV filters.
UV is shown to disrupt skin barrier integrity by increasing TEWL, decreasing skin hydration, promoting SC and epidermal thickness, plus changing skin lipids and proteins levels and structures.4,6,21 Despite the differences in study conditions, the variation of UVR effects on skin barrier-related endpoints remains poorly understood. Haratake et al, demonstrated that UVR (7.5 MED) can lead to a delayed impaired barrier response followed by rapid recovery, which was dependent on epidermal hyperproliferation and inflammation.22 Subsequently, Holleran et al, reported that the same UV dose after 24 hours caused incidence of damaged lamellar bodies (LBs) only at the stratum granulosum (SG) and SC interface, which contributed to the delayed in abnormal barrier permeability and no change in TEWL. Following 72 hours, he observed a deficient lamellar membrane in the lower SC and an increase in impaired LBs at SG/SC interface, causing elevated TEWL and compromised barrier. By 120 hours, there was a hyperproliferative response promoting thickening of the SG and arrival of normal lamellar membranes in the lower SC, which in turn resulted in the restoration of the epidermal barrier.23
In our study, UVR (2 MED) did not cause a drastic change in either TEWL nor hydration (Figure 2A and 2B), which could be attributed to the skin’s ability to delay barrier deficiency and rapidly recover from superficial damage. Nevertheless, treatment with ceramide-containing sunscreen in combination with moisturizer (SPF+Moisturizer) improved skin hydration over time, indicating that the skin water content, which is essential for maintaining barrier function, was both maintained and ameliorated. Moreover, we observed that UVR tended to alter skin surface organization patterns and promote corneocyte maturation (Figure 3 and 4). Out of the three corneocyte microstructural parameters evaluated, UVR significantly increased the appearance of weakly differentiated cells in untreated skin, which persisted up to day 14 and was prevented by treating with the sunscreen or moisturizer alone or in combination (Figure 3C and 3D). This phenomenon is consistent with the ability of UVR to decrease SC cohesion by altering intracellular lipids and corneodesmosomes to compromise barrier integrity.4 Altogether, our findings suggest that an increase in corneocyte maturation was a result of some degree of UV-induced skin barrier damage, disrupting superficial SC morphology. Thus, increased SC turnover or epidermal hyperplasia, as shown in prior studies, are all compensatory mechanisms that the skin barrier utilizes to adapt in response to UV stress to prevent subsequent damage.21–23 Our results indicate that a skincare routine combining a ceramide-containing sunscreen and moisturizer may prevent early UV-induced skin barrier damage and the consequent skin physiological alterations. However, some limitation should be noted. We were unable to compare the efficacy of our ceramidecontaining products with non-ceramide containing sunscreen and moisturizer due to limited test sites on subjects. Future studies will expand on our findings and determine the exact mechanism of CERs capabilities, plus added benefits when combined with UV filters and other ingredients for promoting skin barrier health in response to UV-induced stress.
CONCLUSION
Collectively, our results show that a ceramide-containing
sunscreen and moisturizer routine protects against UV-induced
skin surface barrier changes by preventing erythema and
hyperpigmentation, improving skin hydration, and maintaining
normal superficial skin cells morphology and turnover. In
addition to improving appearance of lesions and minimizing
