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红松皮提取物通过调节 Th1/Th2 平衡和皮肤屏障功能改善 NC/Nga 小鼠的 2,4-二硝基氯苯诱导的特应性皮炎。

Pinus densiflora bark extract ameliorates 2,4-dinitrochlorobenzene-induced atopic dermatitis in NC/Nga mice by regulating Th1/Th2 balance and skin barrier function.

机构信息

Department of Life and Nanopharmaceutical Sciences, Graduate School, Kyung Hee University, 26, Kyungheedae-ro, Dongdaemun-gu, Seoul, 02447, Republic of Korea.

Department of Oriental Pharmaceutical Science, College of Pharmacy, Kyung Hee University, 26, Kyungheedae-ro, Dongdaemun-gu, Seoul, 02447, Republic of Korea.

出版信息

Phytother Res. 2018 Jun;32(6):1135-1143. doi: 10.1002/ptr.6061. Epub 2018 Feb 27.

Abstract

Korean red pine (Pinus densiflora) bark has been traditionally used in Korea and other parts of East Asia to relieve inflammatory diseases. Although many studies using P. densiflora bark have been reported, its effect on atopic dermatitis (AD) has not been elucidated. Thus, we investigated whether the P. densiflora bark extract (PBE) has potential to attenuate AD symptoms and elucidated the molecular mechanism. Oral administration of PBE to mice with 2,4-dinitrochlorobenzene (DNCB)-induced AD lessened dermatitis scores and scratching behavior and significantly reduced measures of epidermal thickness, infiltration of mast cells and eosinophils, levels of immunoglobulin E (IgE), and IgG /IgG ratio in serum. PBE not only inhibited IL-4, IL-5, and IL-13 but also increased IFN-γ in splenic production. Furthermore, PBE significantly suppressed mRNA expression of thymic stromal lymphopoietin and further downregulated the mRNA expression of Th2 and Th17 cytokines such as IL-4, IL-13, IL-17, IL-31, and TNF-α. In addition, the protein expressions of filaggrin, involucrin, and loricrin in lesional skin were recovered by PBE. These results suggest that PBE attenuates DNCB-induced AD via regulating Th1/Th2 balance and skin barrier function.

摘要

韩国红松(Pinus densiflora)树皮在韩国和东亚其他地区被传统用于缓解炎症性疾病。尽管已经报道了许多使用红松树皮的研究,但它对特应性皮炎(AD)的影响尚未阐明。因此,我们研究了红松树皮提取物(PBE)是否具有缓解 AD 症状的潜力,并阐明了其分子机制。用 PBE 对 2,4-二硝基氯苯(DNCB)诱导的 AD 小鼠进行口服给药,可减轻皮炎评分和搔抓行为,并显著降低表皮厚度、肥大细胞和嗜酸性粒细胞浸润、免疫球蛋白 E(IgE)水平以及血清中的 IgG/IgG 比值。PBE 不仅抑制了 IL-4、IL-5 和 IL-13,还增加了脾细胞中 IFN-γ的产生。此外,PBE 还显著抑制了胸腺基质淋巴细胞生成素的 mRNA 表达,并进一步下调了 Th2 和 Th17 细胞因子(如 IL-4、IL-13、IL-17、IL-31 和 TNF-α)的 mRNA 表达。此外,PBE 还恢复了病变皮肤中丝聚蛋白、兜甲蛋白和板层素的蛋白表达。这些结果表明,PBE 通过调节 Th1/Th2 平衡和皮肤屏障功能来减轻 DNCB 诱导的 AD。

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