Standardized extract of Centella asiatica ECa 233 inhibits lipopolysaccharide-induced cytokine release in skin keratinocytes by suppressing ERK1/2 pathways

Objective: To evaluate the effect of standardized extract of Centella asiatica ECa 233 on inflammatory mediator production through cyclooxygenase-2 (COX-2), extracellular signal-regulated kinase 1/2 (ERK1/2) and nuclear factor-κB (NF-κB) pathway in keratinocyte HaCaT cells. Methods: HaCaT cells were...

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Bibliographic Details
Published in:Asian Pacific Journal of Tropical Biomedicine
Main Authors: Furoida Moolsap, Supita Tanasawet, Mayuree H Tantisira, Pilaiwanwadee Hutamekalin, Varomyalin Tipmanee, Wanida Sukketsiri
Format: Article in Journal/Newspaper
Language:English
Published: Wolters Kluwer Medknow Publications 2020
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Online Access:https://doi.org/10.4103/2221-1691.283941
https://doaj.org/article/b144f4dd85cf4e9db77bd00f860fde47
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Summary:Objective: To evaluate the effect of standardized extract of Centella asiatica ECa 233 on inflammatory mediator production through cyclooxygenase-2 (COX-2), extracellular signal-regulated kinase 1/2 (ERK1/2) and nuclear factor-κB (NF-κB) pathway in keratinocyte HaCaT cells. Methods: HaCaT cells were treated with 0.1, 1, 10 and 100 μg/mL ECa 233 in the presence of lipopolysaccharide (LPS). Proinflammatory cytokines and prostaglandin E2 were assessed with ELISA. Western blotting was used to determine the inhibition of COX-2, ERK1/2 and NF-κB protein expression. Results: ECa 233 suppressed LPS-induced release of interleukin- 1β, tumor necrosis factor-α, and prostaglandin E2. ECa 233 also inhibitedCOX-2, phosphorylation of ERK1/2 and the activation of NF-κB. Moreover, the formation of reactive oxygen species (ROS) was decreased in response to LPS-inflamed keratinocytes. Conclusions: ECa 233 inhibits LPS-stimulated production of inflammatory mediators in keratinocytes via suppressing ERK1/2 andNF-κB pathways. The suppressive effect of ECa 233 may be related to an inhibition of ROS production.