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. 2023 Mar 3;8(10):9239-9249.
doi: 10.1021/acsomega.2c07343. eCollection 2023 Mar 14.

Prevention and Repair of Ultraviolet B-Induced Skin Damage in Hairless Mice via Transdermal Delivery of Growth Factors Immobilized in a Gel-in-Oil Nanoemulsion

Yi Zhang  1 , Yuuta Inoue  1 , Jannatul Fardous  2 , Ryota Doi  1 , Takahiro Ijima  3 , Toshioh Fujibuchi  4 , Yo-Ichi Yamashita  5 , Shinichi Aishima  6 , Hiroyuki Ijima  1
Affiliations

Prevention and Repair of Ultraviolet B-Induced Skin Damage in Hairless Mice via Transdermal Delivery of Growth Factors Immobilized in a Gel-in-Oil Nanoemulsion

Yi Zhang et al. ACS Omega. .

Abstract

Ultraviolet (UV) radiation from the sun or artificial sources is one of the primary causes of skin damage, including sunburns, tanning, erythema, and skin cancer. Among the three different types of UV rays, UVB rays have a medium wavelength that can penetrate the epidermal layer of the skin, resulting in sunburn, suntan, blistering, and melanoma in case of chronic exposure. This study aimed to evaluate the preventive and therapeutic effects of a gel-in-oil nanogel dispersion (G/O-NGD) as a transdermal delivery biomolecular carrier for skin damage caused by UVB light. The efficacy of this carrier against UVB-induced skin damage was investigated in vivo by delivering different growth factors (GFs) encapsulated in a G/O-NGD. Artificial UVB light was used to induce skin damage in nude mice, followed by the transdermal application of five GF [vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), transforming growth factor (TGF)-1, and insulin-like growth factor (IGF)-α]-immobilized G/O-NGD. Among these GFs, VEGF and bFGF promoted angiogenesis, while EGF, TGF-1, and IGF-α promoted the repair and regeneration of damaged cells. The results showed that G/O-NGD was superior to heparin-immobilized G/O-NGD in reducing UVB-induced skin damage, such as erythema, epidermal water reduction, inflammation, and dermis thickening. In addition, G/O-NGD could prevent and treat abnormal follicle proliferation caused by UVB rays and exhibited potential to repair lipid glands. Overall, our results demonstrate the potential of G/O-NGDs for the treatment of UVB-induced skin damage.

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Conflict of interest statement

The authors declare no competing financial interest.

Figures

Figure 1
Figure 1
Inhibition of skin erythema and dehydration using the gel-in-oil nanogel dispersion (G/O-NGD) in the prevention group. (A) Images of transtemporal changes on the back skin of mice after ultraviolet (UV)-B irradiation and degree of skin damage with and without application of G/O-NGD. (B) Transcutaneous changes in skin humidity on the back of mice in the prevention group. Data are presented as the mean ± standard deviation. n = 4, *P < 0.05, **P < 0.01. Scale bar = 10 mm.
Figure 2
Figure 2
Inhibition of skin erythema and dehydration using G/O-NGD in the short-term treatment group. (A) Images of transtemporal changes on the back skin of mice after UVB irradiation and degree of skin damage with and without the application of G/O-NGD. (B) Transcutaneous changes in skin humidity on the back of mice in the short-term treatment group. Data are presented as the mean ± standard deviation. n = 4, *P < 0.05, **P < 0.01. Scale bar = 10 mm.
Figure 3
Figure 3
Inhibition of skin erythema and dehydration using G/O-NGD in the long-term treatment group. (A) Images of transtemporal changes on the back skin of mice after UVB irradiation and degree of skin damage with and without the application of G/O-NGD. (B) Transcutaneous changes in skin humidity on the back of mice in the long-term treatment group. Data are presented as the mean ± standard deviation. n = 4, *P < 0.05, **P < 0.01. Scale bar = 10 mm.
Figure 4
Figure 4
CD68 staining of the mouse dorsal skin tissue. (A) Prevention, (B) short-term treatment, and (C) long-term treatment groups. Macrophage counts in the (D) prevention, (E) short-term treatment, and (F) long-term treatment groups. Data are presented as the mean ± standard deviation. n = 4, *P < 0.05, **P < 0.01. Scale bar = 50 μm.
Figure 5
Figure 5
Histological analysis of the mice skin in the no-treatment group. (A) Hematoxylin and eosin (H&E)-stained images of the dorsal skin of mice. (B) Skin tissue fibrosis. (C) Increased number of hair follicles. (D) Inflammation. Scale bar: A = 500 μm; B, C, and D = 200 μm.
Figure 6
Figure 6
Histological analysis of the mice skin in the prevention group. (A) H&E-stained images of the dorsal skin of mice. (B) Epidermal thickness. (C) Dermis thickness. (D) Number of hair follicles. (E) Number of sebaceous glands. Data are presented as the mean ± standard deviation. n = 4, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Scale bar = 100 μm.
Figure 7
Figure 7
Histological analysis of the mice skin in the short-term treatment group. (A) H&E-stained images of the dorsal skin of mice. (B) Epidermal thickness. (C) Dermis thickness. (D) Number of hair follicles. (E) Number of sebaceous glands. Data are presented as the mean ± standard deviation. n = 4, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Scale bar = 100 μm.
Figure 8
Figure 8
Histological analysis of the mice skin in the long-term treatment group. (A) H&E-stained images of the dorsal skin of mice. (B) Epidermal thickness. (C) Dermis thickness. (D) Number of hair follicles. (E) Number of sebaceous glands. Data are presented as the mean ± standard deviation. n = 4, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Scale bar = 100 μm.
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