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提取物可预防二硝基氯苯诱导的小鼠特应性皮炎。

extract prevents atopic dermatitis in DNCB-induced mice.

作者信息

Choi JeongUn, Jang A-Yeong, Rod-In Weerawan, Lee Dae-Hee, Choi Ki Young, Park Woo Jung

机构信息

Department of Marine Bio Food Science, Gangneung-Wonju National University, Gangneung, Gangwon 25457 Republic of Korea.

Department of Agricultural Science, Faculty of Agriculture Natural Resources and Environment, Naresuan University, Phitsanulok, 65000 Thailand.

出版信息

Food Sci Biotechnol. 2024 Feb 29;33(11):2643-2652. doi: 10.1007/s10068-024-01523-1. eCollection 2024 Aug.

Abstract

Atopic dermatitis (AD) is a chronic inflammatory-allergic skin disorder that causes pruritic and eczematous skin lesions. Effect of extract (CFE) on AD has not been reported yet. In this study, inhibitory effects of CFE against skin severity scores, skin lesions, AD characteristics, and histological features of BALB/c mice with AD caused by 2,4-dinitrochlorobenzene (DNCB) were investigated. Results indicated that AD effects of CFE reduced body, skin, ear, spleen, thymus, and lymph node weights. Histopathological changes in skin reactions on the back and ears showed that CFE inhibited thickening of the epidermis and ear. Moreover, CFE reduced epidermal swelling and ear thickness compared with the DNCB group. These results suggest that CFE might be effective in alleviating AD with potential as a promising candidate for therapeutic and cosmetic treatment of inflammatory dermatitis. CFE may be useful in alleviating AD and could be a potential treatment for inflammatory dermatitis.

摘要

特应性皮炎(AD)是一种慢性炎症性过敏性皮肤病,会导致皮肤出现瘙痒性和湿疹性病变。目前尚未有关于提取物(CFE)对AD影响的报道。在本研究中,研究了CFE对由2,4-二硝基氯苯(DNCB)引起的AD的BALB/c小鼠的皮肤严重程度评分、皮肤病变、AD特征和组织学特征的抑制作用。结果表明,CFE对AD的影响降低了身体、皮肤、耳朵、脾脏、胸腺和淋巴结的重量。背部和耳朵皮肤反应的组织病理学变化表明,CFE抑制了表皮和耳朵的增厚。此外,与DNCB组相比,CFE减轻了表皮肿胀和耳朵厚度。这些结果表明,CFE可能有效缓解AD,有潜力成为治疗和美容治疗炎症性皮炎的有前景的候选药物。CFE可能有助于缓解AD,并且可能是炎症性皮炎的一种潜在治疗方法。

相似文献

1
extract prevents atopic dermatitis in DNCB-induced mice.提取物可预防二硝基氯苯诱导的小鼠特应性皮炎。
Food Sci Biotechnol. 2024 Feb 29;33(11):2643-2652. doi: 10.1007/s10068-024-01523-1. eCollection 2024 Aug.

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