Artemisinin triggers induction of cell-cycle arrest and apoptosis in Leishmania donovani promastigotes

J Med Microbiol. 2007 Sep;56(Pt 9):1213-1218. doi: 10.1099/jmm.0.47364-0.

Abstract

A major impediment to effective anti-leishmanial chemotherapy is the emergence of drug resistance, especially to sodium antimony gluconate, the first-line treatment for leishmaniasis. Artemisinin, a sesquiterpene lactone isolated from Artemisia annua, is an established anti-malarial compound that showed anti-leishmanial activity in both promastigotes and amastigotes, with IC(50) values of 160 and 22 microM, respectively, and, importantly, was accompanied by a high safety index (>22-fold). The leishmanicidal activity of artemisinin was mediated via apoptosis as evidenced by externalization of phosphatidylserine, loss of mitochondrial membrane potential, in situ labelling of DNA fragments by terminal deoxyribonucleotidyltransferase-mediated dUTP nick end labelling (TUNEL) and cell-cycle arrest at the sub-G(0)/G(1) phase. Taken together, these data indicate that artemisinin has promising anti-leishmanial activity that is mediated by programmed cell death and, accordingly, merits consideration and further investigation as a therapeutic option for the treatment of leishmaniasis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antiprotozoal Agents / pharmacology*
  • Apoptosis*
  • Artemisinins / pharmacology*
  • Cell Cycle / drug effects*
  • Cell Membrane / chemistry
  • DNA Breaks, Single-Stranded
  • Humans
  • In Situ Nick-End Labeling
  • Inhibitory Concentration 50
  • Leishmania donovani / cytology
  • Leishmania donovani / drug effects*
  • Membrane Potential, Mitochondrial / drug effects
  • Phosphatidylserines / analysis

Substances

  • Antiprotozoal Agents
  • Artemisinins
  • Phosphatidylserines
  • artemisinin