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Standardized extract of Centella asiatica ECa 233 inhibits lipopolysaccharide-induced cytokine release in skin keratinocytes by suppressing ERK1/2 pathways
Furoida Moolsap1, Supita Tanasawet2, Mayuree H Tantisira3, Pilaiwanwadee Hutamekalin4, Varomyalin Tipmanee5, Wanida Sukketsiri1
1 Department of Pharmacology, Faculty of Science, Prince of Songkla University, Songkhla, 90110, Thailand
2 Department of Anatomy, Faculty of Science, Prince of Songkla University, Songkhla, 90110, Thailand
3 Faculty of Pharmaceutical Science, Burapha University, Chon Buri Campus, Chon Buri, 20131, Thailand
4 Department of Physiology, Faculty of Science, Prince of Songkla University, Songkhla, 90110, Thailand
5 Department of Biomedical Sciences, Faculty of Medicine, Prince of Songkla University, Songkhla, 90110, Thailand
Correspondence Address:
Wanida Sukketsiri
Department of Pharmacology, Faculty of Science, Prince of Songkla University, Songkhla, 90110
Thailand
 Source of Support: The accomplishment of this study was supported by grant from
the General Project and Invention of Prince of Songkla University
(SCI600421S) and Graduate School of Prince of Songkla University,
Songkhla, Thailand, Conflict of Interest: None  | 2 |
DOI: 10.4103/2221-1691.283941
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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.
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