The anti-inflammatory effect of PHBV/Collagen (PHCP) was examined in a mouse model of lipopolysaccharide (LPS)-induced skin inflammation. Vascular permeability on the back skin was measured by the local accumulation of Evan’s blue dye after subcutaneous injection of LPS (30 µg site^-1 ). Dye leakage in the skin showed a significant increase at 2 h after injection of LPS. This LPS-induced dye leakage was also completely inhibited by HO-1 inhibitor, ZnPP, and antioxidants, including methyl gallate, trolox, and mannitol. To study the possible mechanisms underlying the in vivo anti-inflammatory effect of PHCP against LPS-induced inflammation, we also examined the effects of PHCP on malondialdehyde (MDA) and glutathione levels in skin tissues and found that pretreatment with PHCP resulted in inhibited MDA elevation and a remarkable reduction of glutathione level. In addition, similar results were obtained after pretreatment with antioxidants, including trolox and mannitol, and HO-1 inhibitor, ZnPP. Histopathologically, an influx of neutrophils into the skin dermis was detected between 24 h and 72 h after LPS injection (30, 100 µg site^-1), compared to control animals after injection of saline. This increase was greater in mice treated with 100 µg of LPS than in those treated with 30 µg of LPS and was significantly suppressed by pretreatment with PHCP, antioxidants, and HO-1 inhibitor. These results collectively suggest that PHCP has an anti-inflammatory effect against LPS-induced inflammation model in vivo and may be a good candidate for the skin tissue engineering biomedical application primarily through manipulation of the redox state.

The aim of this study was to evaluate the alleviative effects of a nude pack containing black tea water extract (NPBT) on inflammation and skin barrier damage in hairless mice. Skin inflammation and skin barrier damage were induced by UVB irradiation to the backs of hairless mice for five weeks. And, at the same time, saline (C), NPBT (1%: E1, 2%: E2), and 0.01% retinoic acid diluted with polyethylene glycol (PC) were applied topically twice per day, five days per week, for a period of five weeks. The skin erythema indices of the E1 and E2 groups were significantly lower (p<0.05) than those of the C group through one week after the beginning of the experiment. Meanwhile, water contents of the E1 and E2 groups were significantly higher (p<0.05) than those of the C group through two weeks after the beginning of the experiment. Remarkable thickening of epidermis and dermis was observed in the C group, compared with the PC, E1, or E2 groups. In the C group, infiltration of many inflammatory cells, including neutrophils and lymphocytes, was observed in dermis and a large number of mast cells were observed in dermis and hypodermis, and the degree of degranulation was remarkable. However, these phenomena were alleviated in the PC, E1, and E2 groups. Therefore, NPBT could have considerable inhibitory efficacy on inflammation and skin barrier damage induced by UVB irradiation.

Avocado, superfood, contains a variety of essential nutrients and phytochemicals. The purpose of this study was to explore whether avocado could modulate skin inflammation in vivo. We elucidated the pharmacological effects of avocado on compound 48/80- or histamine-induced scratching behaviors and 2, 4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis (AD)-like skin lesions in mice. Additionally, we investigated the anti-inflammatory activity of avocado and its underlying mechanism including its effect on the expression levels of inflammatory-related genes and nuclear factor -κB (NF-κB) in DNCB-induced AD-like skin lesions. The findings of this study demonstrate that avocado attenuated AD clinical symptoms including itching, eczematous, erythema and dryness and histamine levels in mice. Moreover, avocado suppressed both inflammatory cytokines expression as well as NF-κB and caspase-1 activation in AD-like skin lesions in mice. Taken together, these results demonstrate that avocado may be a potential candidate for treating skin inflammatory diseases like AD.

제니스테인(genistein)은 대두에서 추출한 대표적인 이소 플라본 화합물 중 하나이며 노화 방지 및 항염 증 활성 효과에 대한 연구가 많이 이뤄졌다. 그러나 제니스테인은 유기용매에 높은 용해도를 보일지라도 물에 대한 수용성은 매우 낮아 생체이용률이 떨어진다. 따라서 본 연구에서는 제니스테인의 수용성과 안정성이 크게 향상된 제니스테인 cyclodextrin 포접체(genistein CD complex)를 제니스테인과 직접 비교 분석하고자 하였다. 우선 세포독성 실험을 위해 RAW264.7 대식세포를 대상으로 CCK-8 assay를 시행하였고, 제니스테인 및 제니스테인 cyclodextrin 포접체 모두 10 μ g/mL 농도부터 세포독성이 나타나 최대 농도는 10 μ g/mL로 설정 하고 실험을 진행하였다. LPS에 의해 활성화 된 RAW264.7 세포에서 NO(nitric oxide) 생성 및 iNOS mRNA 발현을 관찰한 결과 제니스테인 CD 포접체가 제니스테인 자체 보다 더 효과적으로 억제하였다. 또한 IL1-α, IL1-β, IL-6 및 TNF-α와 같은 염증성 사이토카인의 mRNA 발현이 농도 의존적으로 감소됨을 확인하였다. 이 뿐 아니라 인간 각질형성세포인 HaCaT 세포를 이용해 TEER 및 피부장벽 강화 효과를 관찰한 결과 제니스 테인 CD 포접체 처리군에서 TEER이 농도 의존적으로 증가되었고, 세포 이동 실험에서도 동일한 결과를 얻을 수 있었다. 따라서 제니스테인 CD 포접체에 대한 피부 재생 및 장벽 강화에 관한 임상 연구등이 수행된다면, 효과적인 아토피 피부염 또는 피부장벽 개선 기능성 화장품 원료로 사용될 수 있을 것으로 기대된다.

자외선은 외부적인 스트레스 자극인자로 작용하여 사람 각질형성세포에서 reactive oxygen species (ROS)와 비활성 코르티손을 활성 코르티솔로 전환시키는 효소인 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1)의 발현 및 활성을 증가시킨다고 알려져 있다. 또한, ROS가 증가된 피부에서는 염증 유발 사이토카인과 염증 매개 인자의 발현이 증가되어 결과적으로 염증반응을 일으키게 되는 원인이 된다. 본 연구에서는 각질형성세포(HaCaT)에서 11β-HSD1 억제제가 ROS 분해효소인 catalase의 생성을 회복시킴에 착안하여, 11β-HSD1의 발현을 저해함과 동시에 ROS로부터 유도되는 염증 반응을 억제하는 천연물 소재를 발굴하고자 하였다. 그 중 능실 추출물과 그 분획물은 각각 11β-HSD1의 발현과 ROS 생성 증가를 억제하고, 염증성 사이토카인인 tumor necrosis factor (TNF)-α, interleukin (IL)-1α, -1β의 발현을 억제하였다. 또한, 자외선에 의해 유도되는 염증 매개인자인 cyclooxygenase (COX)-2, inducible nitric oxide synthase (iNOS), prostaglandin E2 (PGE2)의 생성을 저해하였다. 따라서 본 연구 결과로부터 능실 추출물 및 그 분획물은 11β-HSD1의 발현을 억제함과 동시에 ROS에 의해 유발된 피부 염증 반응을 효과적으로 저해함을 확인하였다.