Centella asiatica phytochemical Madecassoside enhances skin wound healing and protects against UVB-induced keratinocyte damage.

IF 3.6 Q2 MEDICINE, RESEARCH & EXPERIMENTAL
Tadhi Sucharitakul, Pimngeon Chatkul, Wilasinee Satianrapapong, Apiwan Arinno, Wanapas Wachiradejkul, Suticha Kittayaruksakul, Jaturon Kwanthongdee, Saimai Chatree, Anyamanee Chatsirisupachai, Pawin Pongkorpsakol
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Abstract

Madecassoside, one of the main bioactive compounds found in Centella asiatica extract, has long been used in the cosmetic regime for skin care with doubtful effects. The main objectives of this study are to investigate the effects of Madecassoside on skin wound healing, UVB-induced keratinocyte damages, and to search for its pharmacological mechanism. Here, using fully differentiated keratinocyte-like HaCaT cell monolayers as an in vitro model, we found that Madecassoside enhanced wound healing and protected against UVB-induced keratinocyte apoptosis and reduction of cell viability. Indeed, these pharmacological effects of Madecassoside were completely abolished by pretreatment of an intracellular Ca2+ chelator (BAPTA), inhibitors of AMP-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR), and extracellular signal-regulated kinase (ERK). In addition, our Western blotting analyses strongly indicated that Madecassoside-induced ERK phosphorylation was suppressed by pretreatment of BAPTA, inhibitors of AMPK and mTOR signaling. Collectively, these data suggested that Madecassoside promotes wound healing and reduces keratinocyte apoptosis after being damaged by UVB radiation, at least in part, via Ca2+/AMPK- and mTOR-dependent ERK phosphorylation.

积雪草植物化学成分马尾皂苷促进皮肤伤口愈合,防止uvb诱导的角质细胞损伤。
积雪草皂苷是积雪草提取物中发现的主要生物活性化合物之一,长期以来一直用于护肤美容,效果可疑。本研究的主要目的是研究麻花皂苷对皮肤创面愈合、uvb诱导的角质细胞损伤的影响,并探讨其药理机制。在这里,我们使用完全分化的角化细胞样HaCaT细胞单层作为体外模型,我们发现麻花皂苷可以促进伤口愈合,防止uvb诱导的角化细胞凋亡和细胞活力降低。事实上,madecasoside的这些药理作用通过细胞内Ca2+螯合剂(BAPTA)、amp活化蛋白激酶(AMPK)抑制剂、哺乳动物雷帕霉素靶点(mTOR)和细胞外信号调节激酶(ERK)的预处理完全消除。此外,我们的Western blotting分析强烈表明,madecassoside诱导的ERK磷酸化被BAPTA预处理、AMPK和mTOR信号抑制剂抑制。总的来说,这些数据表明,madecas皂苷促进伤口愈合,减少受UVB辐射损伤后角质细胞凋亡,至少部分是通过Ca2+/AMPK-和mtor依赖性ERK磷酸化。
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来源期刊
Tissue Barriers
Tissue Barriers MEDICINE, RESEARCH & EXPERIMENTAL-
CiteScore
6.60
自引率
6.50%
发文量
25
期刊介绍: Tissue Barriers is the first international interdisciplinary journal that focuses on the architecture, biological roles and regulation of tissue barriers and intercellular junctions. We publish high quality peer-reviewed articles that cover a wide range of topics including structure and functions of the diverse and complex tissue barriers that occur across tissue and cell types, including the molecular composition and dynamics of polarized cell junctions and cell-cell interactions during normal homeostasis, injury and disease state. Tissue barrier formation in regenerative medicine and restoration of tissue and organ function is also of interest. Tissue Barriers publishes several categories of articles including: Original Research Papers, Short Communications, Technical Papers, Reviews, Perspectives and Commentaries, Hypothesis and Meeting Reports. Reviews and Perspectives/Commentaries will typically be invited. We also anticipate to publish special issues that are devoted to rapidly developing or controversial areas of research. Suggestions for topics are welcome. Tissue Barriers objectives: Promote interdisciplinary awareness and collaboration between researchers working with epithelial, epidermal and endothelial barriers and to build a broad and cohesive worldwide community of scientists interesting in this exciting field. Comprehend the enormous complexity of tissue barriers and map cross-talks and interactions between their different cellular and non-cellular components. Highlight the roles of tissue barrier dysfunctions in human diseases. Promote understanding and strategies for restoration of tissue barrier formation and function in regenerative medicine. Accelerate a search for pharmacological enhancers of tissue barriers as potential therapeutic agents. Understand and optimize drug delivery across epithelial and endothelial barriers.
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