Topical hesperidin prevents glucocorticoid‐induced abnormalities in epidermal barrier function in murine skin

Man, George; Mauro, Theodora M.; Kim, Peggy L.; Hupe, Melanie; Zhai, Yongjiao; Sun, Richard; Crumrine, Debbie; Cheung, Carolyn; Nuño-González, Almudena; Elias, Peter M.; Man, Mao‐Qiang

doi:10.1111/exd.12480

Cited by 28 publications

(30 citation statements)

References 84 publications

(104 reference statements)

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“…Localized weak PCNA immunoreactivity in few cells of both stratum basale and ORS of atrophied hair follicles was confirmed statistically and was previously reported as marked reduction of PCNA-positive cells in GC-treated epidermis [23] . Also, weak CK19 immunoreactivity was confirmed statistically, it was in agreement with previous study which detected that after GC application keratinocyte proliferation and hair follicles was almost completely blocked and resulted in significant epidermal hypoplasia [24] .…”

Section: Discussionsupporting

confidence: 80%

Effect of Curcumin versus Hyaluronic Acid on Glucocorticoid Induced Skin Atrophy and Subsequent Skin Abrasions in Rats

Fawzy

Ahmed

Elshafie

et al. 2019

Egyptian Journal of Histology

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Background: Skin is the largest organ of the body in surface area and weight. One of the most important side effects of topical glucocorticoids therapy is skin atrophy. This study aimed to evaluate the possible therapeutic effects of curcumin versus aftamed gel (Hyaluronic Acid) on glucocorticoid-induced skin atrophy, as well as on subsequently induced abrasion wounds. Methods: Forty two adult male albino rats were divided into 4 groups: Group1 (Control group) of 6 rats, Group II (Steroid-Exposed Group), Group III (Curcumin-Treated Group) and Group IV (Aftamed-treated group). Each of group II, III and IV were subdivided into two subgroups IIA, IIIA, IVA (subjected to clobetasol propionate cream) each included 6 rats and IIB, IIIB, IVB (subjected to clobetasol propionate cream, then exposed to skin abrasion) each included 6 rats. Skin biopsies were taken from the dorsum of rats 12th days from the stoppage of clobetasol propionate application. Sections were stained with hematoxylin and eosin, Masson's trichrome and immunohistochemichal stain for PCNA & CK19. Epidermal thicknesses, mean area percent of collagen fibers and mean number of PCNA & CK19 immunopositive cells were measured. Results: Steroid-exposed group showed thinning of epidermal and dermal layers with scanty hair follicles and sebaceous glands as well as delay in wound healing. Increased epidermal thickness and reorganized dermal structural elements with increased PCNA & CK19 immunopositive cells were more obvious in curcumin treated group than aftamed treated group. Conclusion: topical application of curcumin had more improving effect on skin and its abrasions rather than aftamed gel.

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Section: Discussionsupporting

confidence: 80%

Effect of Curcumin versus Hyaluronic Acid on Glucocorticoid Induced Skin Atrophy and Subsequent Skin Abrasions in Rats

Fawzy

Ahmed

Elshafie

et al. 2019

Egyptian Journal of Histology

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“…Hence, comparable topical acidification strategies should also benefit adults with inflammatory dermatoses, who have a prior history of AD. It is important to note that acidification can be impacted either directly or indirectly, for example, by topical agents, such as PPARs and bioflavonoids that we have shown enhance NHE1 and sPLA2 expression …”

Section: Clinical Implications Of Sc Acidificationmentioning

confidence: 99%

The how, why and clinical importance of stratum corneum acidification

Elias

2017

Experimental Dermatology

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In this article, I review the multiple endogenous mechanisms that contribute to the highly acidic pH of normal stratum corneum (SC). Then, I describe how each mechanism potentially impacts specific defensive functions of the SC. Finally, I review the rapidly expanding, clinical implications and potential therapeutic applications of SC acidification. K E Y W O R D Sacidification, barrier function, pH, stratum corneum 1000 | ELIAS review the four established, endogenous mechanisms and then present evidence in support of a likely fifth mechanism. | Mechanism 1During terminal differentiation, phospholipids are fully hydrolysed to their constituent FFA by secretory phospholipases (sPLA2). Studies with pharmacologic inhibitors [8] and in transgenic mice with deletions in the pla2g2f isoform of sPLA2 [9] show that phospholipid-derived FFA account for ≈one unit of SC bulk pH, but also that these FFA simultaneously become necessary components of the lamellar bilayers that mediate the permeability barrier. [8] Yet, whether the sPLA2 mechanism selectively acidifies only extracellular domains and/or whether it also impacts the pH within the corneocyte cytosol is not known. | Mechanism 2In transgenic mice with a selective knockout of the sodium-hydrogen antiporter type 1 (NHE1), the bulk pH of the SC increases by only ≈1/4 pH unit.[4] Yet, this mechanism selectively acidifies extracellular domains in the lower SC, the key site where both barrier function and SC cohesion initially become established, and where the earliest events leading to desquamation also are initiated.[10] Pertinently, the enzymes that regulate these functions all are lamellar bodyderived products that are delivered to extracellular domains as the contents of these organelles are secreted. Of these enzymes, two are ceramide-generating hydrolases, β-glucocerebrosidase and acidic sphingomyelinase, which both require an acidic pH for optimal activity. Conversely, the extracellular kallikreins (KLKs) that initiate desquamation remain inactive at a reduced pH. [11] Together, the colocalization of a low pH along with secreted hydrolytic enzymes explains the impact of this acidifying mechanism on barrier function, SC cohesion and desquamation. | Mechanism 3The catabolism of filaggrin (FLG) into its constituent amino acids, followed by the further, downstream deimination of these amino acids into polycarboxylic acids, [6] including trans-urocanic acid, accounts for about ½ unit of the bulk pH of the SC. The best evidence for this link is the pH changes that accompany loss-of-function mutations in FLG in ichthyosis vulgaris (IV), where single-allele mutations result in a ¼ unit increase in pH, while double-allele loss of function results in a ½ unit increase in surface pH. [12] If the protons generated via this mechanism remain largely localized to the corneocyte cytosol, they likely would suppress one or more KLKs, which exhibit neutral to alkaline pH optima. These KLKs in turn activate IL-1α and IL-1β as the pH of the SC increases following external insu...

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“…Eighteen hours after the last NO treatment, basal epidermal permeability barrier function was assessed by measuring transepidermal water loss rates (TEWL), using TM300 connected to MPA5 (C&K, Cologne, Germany). [ 14 ] For barrier recovery in mice, TEWL was measured 0, 2 and 4 hours after tape stripping for 3 times (10‐fold increase in TEWL measured with a Meeco electrolytic moisture analyser or over twofold increase measured with TM300. see figure legend of Figure 1), and per cent barrier recovery was calculated as described earlier.…”

Section: Experimental Designmentioning

confidence: 99%

Inducible nitric oxide synthase is required for epidermal permeability barrier homeostasis in mice

Dang

Man

Zhang

et al. 2020

Experimental Dermatology

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Nitric oxide (NO) regulates a variety of epidermal functions, including epidermal proliferation, differentiation and cutaneous wound healing. However, whether nitric oxide (NO) and its synthetic enzymes regulate epidermal permeability barrier homeostasis is not clear. In the present study, we employed inducible nitric oxide synthase (iNOS) KO mice to explore the role of iNOS in epidermal permeability barrier homeostasis. Our results showed that iNOS mice displayed a comparable levels of basal transepidermal water loss rates, stratum corneum hydration and skin surface pH to their wild‐type mice, but epidermal permeability barrier recovery was significantly delayed both 2 and 4 hours after acute barrier disruption by tape stripping. In parallel, expression levels of mRNA for epidermal differentiation‐related proteins and lipid synthetic enzymes were lower in iNOS KO mice versus wild‐type controls. Topical applications of two structurally unrelated NO donors to iNOS KO mice improved permeability barrier recovery kinetics and upregulated expression levels of mRNA for epidermal differentiation‐related proteins and lipid synthetic enzymes. Together, these results indicate that iNOS and its product regulate epidermal permeability barrier homeostasis in mice.

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Topical hesperidin prevents glucocorticoid‐induced abnormalities in epidermal barrier function in murine skin

Cited by 28 publications

References 84 publications

Effect of Curcumin versus Hyaluronic Acid on Glucocorticoid Induced Skin Atrophy and Subsequent Skin Abrasions in Rats

Effect of Curcumin versus Hyaluronic Acid on Glucocorticoid Induced Skin Atrophy and Subsequent Skin Abrasions in Rats

The how, why and clinical importance of stratum corneum acidification

Inducible nitric oxide synthase is required for epidermal permeability barrier homeostasis in mice

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