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用绿茶多酚(-)-表没食子儿茶素-3-没食子酸酯处理小鼠皮肤可预防紫外线B诱导的白细胞浸润、抗原呈递细胞耗竭和氧化应激。

Green tea polyphenol (-)-epigallocatechin-3-gallate treatment to mouse skin prevents UVB-induced infiltration of leukocytes, depletion of antigen-presenting cells, and oxidative stress.

作者信息

Katiyar S K, Mukhtar H

机构信息

Department of Dermatology, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA.

出版信息

J Leukoc Biol. 2001 May;69(5):719-26.

Abstract

Ultraviolet (UV) radiation-induced infiltrating leukocytes, depletion of antigen-presenting cells, and oxidative stress in the skin play an important role in the induction of immune suppression and photocarcinogenesis. Earlier we have shown that topical application of polyphenols from green tea or its major chemopreventive constituent (-)-epigallocatechin-3-gallate (EGCG) prevents UV-B-induced immunosuppression in mice. To define the mechanism of prevention, we found that topical application of EGCG (3 mg/mouse/3 cm(2) of skin area) to C3H/HeN mice before a single dose of UV-B (90 mJ/cm(2)) exposure inhibited UV-B-induced infiltration of leukocytes, specifically the CD11b+ cell type, and myeloperoxidase activity, a marker of tissue infiltration of leukocytes. EGCG treatment was also found to prevent UV-B-induced depletion in the number of antigen-presenting cells when immunohistochemically detected as class II MHC+ Ia+ cells. UV-B-induced infiltrating cell production of H2O2 and nitric oxide (NO) was determined as a marker of oxidative stress. We found that pretreatment of EGCG decreased the number of UV-B-induced increases in H2O2-producing cells and inducible nitric oxide synthase-expressing cells and the production of H2O2 and NO in both epidermis and dermis at a UV-B-irradiated site. Together, these data suggest that prevention of UV-B-induced infiltrating leukocytes, antigen-presenting cells, and oxidative stress by EGCG treatment of mouse skin may be associated with the prevention of UV-B-induced immunosuppression and photocarcinogenesis.

摘要

紫外线(UV)辐射诱导的皮肤浸润性白细胞、抗原呈递细胞耗竭以及氧化应激在免疫抑制诱导和光致癌过程中起重要作用。此前我们已表明,局部应用绿茶中的多酚或其主要化学预防成分(-)-表没食子儿茶素-3-没食子酸酯(EGCG)可预防小鼠紫外线B(UV-B)诱导的免疫抑制。为明确预防机制,我们发现,在单次UV-B(90 mJ/cm²)照射前,对C3H/HeN小鼠局部应用EGCG(3 mg/小鼠/3 cm²皮肤面积)可抑制UV-B诱导的白细胞浸润,特别是CD11b⁺细胞类型,以及髓过氧化物酶活性,髓过氧化物酶活性是白细胞组织浸润的标志物。当通过免疫组织化学检测为II类主要组织相容性复合体(MHC)⁺ Ia⁺细胞时,还发现EGCG处理可预防UV-B诱导的抗原呈递细胞数量减少。测定UV-B诱导的浸润细胞产生过氧化氢(H₂O₂)和一氧化氮(NO)作为氧化应激的标志物。我们发现,EGCG预处理可减少UV-B诱导的H₂O₂产生细胞和诱导型一氧化氮合酶表达细胞数量增加,以及UV-B照射部位表皮和真皮中H₂O₂和NO的产生。总之,这些数据表明,EGCG处理小鼠皮肤预防UV-B诱导的浸润性白细胞、抗原呈递细胞和氧化应激可能与预防UV-B诱导的免疫抑制和光致癌有关。

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