4.7 Article

Pharmacokinetics and metabolomics investigation of an orally modified formula of standardized Centella asiatica extract in healthy volunteers

Journal

SCIENTIFIC REPORTS
Volume 11, Issue 1, Pages -

Publisher

NATURE PORTFOLIO
DOI: 10.1038/s41598-021-86267-2

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Funding

  1. 100th Anniversary Chulalongkorn University Fund for Doctoral Scholarship
  2. 90th Anniversary Chulalongkorn University Fund (Ratchadaphiseksomphot Endowment Fund)

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The modified formula of ECa 233 affects its disposition kinetics in the body and alters the human metabolome. After oral administration of ECa 233, accumulation of asiatic acid and an increase in choline were observed, which may be beneficial for mitigating cognitive impairment.
The formula of a standardized extract of Centella asiatica (ECa 233) was modified to improve its dissolution, with implications for pharmacokinetics and metabolomic profile. This study aimed to understand the resultant changes in disposition kinetics of ECa 233 and alterations to human metabolome after oral administration. This study was a two-sequence of dosages (250 and 500 mg), with an open-label phase I clinical trial. The modified formula was administered in single and multiple doses to twelve healthy Thai volunteers. The major parent compounds, madecassoside and asiaticoside, were rarely absorbed, instead undergoing biotransformation into active metabolites, madecassic acid and asiatic acid with possibility to be eliminated via fecal route. Increasing the dose of ECa 233 resulted in significantly greater plasma levels of those active metabolites, with accumulation of asiatic acid after multiple oral administration for seven days. Examining the impacts of accumulation behavior on metabolomics, the study traced changes in levels pre- and post-dose of five relevant human metabolites. Administration of ECa 233 was found to be significantly associated with an increase of choline, an endogenous metabolite with documented benefits for learning and memory. Therefore, ECa 233 may be useful in mitigating cognitive impairment, through its role in modulating human metabolites.

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