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黄芪甲苷IV通过抑制Fas/Fas L介导的凋亡信号通路对脱发的有益作用。

Beneficial effects of Astragaloside IV for hair loss via inhibition of Fas/Fas L-mediated apoptotic signaling.

作者信息

Kim Mi Hye, Kim Sung-Hoon, Yang Woong Mo

机构信息

College of Korean Medicine and Institute of Korean Medicine, Kyung Hee University, Seoul, Korea.

Cancer Preventive Material Development Research Center, College of Korean Medicine, Kyung Hee University, Seoul, Korea.

出版信息

PLoS One. 2014 Mar 27;9(3):e92984. doi: 10.1371/journal.pone.0092984. eCollection 2014.

Abstract

Apoptosis with premature termination of hair follicle growth induces several types of hair loss and is one of the crucial factors of hair loss. Astragaloside IV, which is a major component of Astragalus membranaceus, is a cycloartane triterpene saponin. Although an anti-apoptotic effect of Astragaloside IV has been reported, its effects against hair loss have not been investigated. To explore the underlying mechanisms of Astragaloside IV on apoptotic signaling in hair follicle, the dorsal skin of depilated C57BL/6 mice was topically treated with 1 and 100 μM Astragaloside IV for 14 days. In Astragaloside IV-treated group, TUNEL-positive cells were reduced. We found that Astragaloside IV blocked the procaspase-8, resulting in the inhibition of caspase-3 and procaspase-9 activities. The changes were accompanied with down-regulation of Bax and p53, and up-regulation of Bcl-2 and Bcl-xL by Astragaloside IV treatment. In addition, activation of NF-κB and phosphorylation of IκB-α were inhibited, along with decreases in three MAPKs: ERK, SAPK/JNK and p38 by Astragaloside IV. The expressions of KGF, p21, TNF-α and IL-1β, which are keratinocyte terminal differentiation markers associated with catagen, were modulated by treatment with Astragaloside IV. These results demonstrated that Astragaloside IV is concerned with blocking the Fas/Fas L-mediated apoptotic pathway, which would be an alternative therapy for hair loss.

摘要

毛囊生长过早终止导致的细胞凋亡会引发多种类型的脱发,是脱发的关键因素之一。黄芪甲苷IV是黄芪的主要成分,属于环阿尔廷烷型三萜皂苷。尽管已有报道黄芪甲苷IV具有抗凋亡作用,但其对脱发的影响尚未得到研究。为探究黄芪甲苷IV对毛囊凋亡信号传导的潜在机制,将1 μM和100 μM的黄芪甲苷IV局部涂抹于脱毛的C57BL/6小鼠背部皮肤,持续14天。在黄芪甲苷IV治疗组中,TUNEL阳性细胞减少。我们发现黄芪甲苷IV可阻断procaspase-8,从而抑制caspase-3和procaspase-9的活性。这些变化伴随着黄芪甲苷IV处理后Bax和p53的下调以及Bcl-2和Bcl-xL的上调。此外,黄芪甲苷IV抑制了NF-κB的激活和IκB-α的磷酸化,同时降低了三种丝裂原活化蛋白激酶(MAPKs):细胞外调节蛋白激酶(ERK)、应激激活蛋白激酶/应激活化蛋白激酶(SAPK/JNK)和p38。黄芪甲苷IV处理可调节与退行期相关的角质形成细胞终末分化标志物角质形成细胞生长因子(KGF)、p21、肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)的表达。这些结果表明,黄芪甲苷IV与阻断Fas/Fas L介导的凋亡途径有关,这可能成为脱发的一种替代治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aebe/3968031/ec5476935cef/pone.0092984.g001.jpg

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