Centella asiatica phytochemical Madecassoside enhances skin wound healing and protects against UVB-induced keratinocyte damage
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Issued Date
2025-01-01
Resource Type
ISSN
21688362
eISSN
21688370
Scopus ID
2-s2.0-105010959832
Journal Title
Tissue Barriers
Rights Holder(s)
SCOPUS
Bibliographic Citation
Tissue Barriers (2025)
Suggested Citation
Sucharitakul T., Chatkul P., Satianrapapong W., Arinno A., Wachiradejkul W., Kittayaruksakul S., Kwanthongdee J., Chatree S., Chatsirisupachai A., Pongkorpsakol P. Centella asiatica phytochemical Madecassoside enhances skin wound healing and protects against UVB-induced keratinocyte damage. Tissue Barriers (2025). doi:10.1080/21688370.2025.2532229 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/111363
Title
Centella asiatica phytochemical Madecassoside enhances skin wound healing and protects against UVB-induced keratinocyte damage
Corresponding Author(s)
Other Contributor(s)
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 Ca<sup>2+</sup> 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 Ca<sup>2+</sup>/AMPK- and mTOR-dependent ERK phosphorylation.