Pengaruh Paparan Artemisinin terhadap Ekspresi Gen PArt pada Plasmodium falciparum Galur Papua 2300

Abstract

no new therapeutic medicine to replace artemisinin. Even though the mechanism of artemisinin resistance has not been clearly understood, the resistance of P. falciparum towards the antimalaria artemisinin may occur due to the influence of by the internal factors of P. falciparum, including the induction of the protein-expressing gene expression. One of the genes is the Triptophan-rich Protein (PArt) gene that is important in the membrane-spanning protein and plays a role in protein folding to maintain hydrophobic contact.. This study aimed to prove that Triptophan-rich Protein overexspression in P. falciparum Papua 2300 strain may cause repeated artemisin exposure in vitro. This study was performed in a period from February to November 2013 in Infection and Tropical Diseases Hospital, Airlangga University. The design used was experimental study with post-test only control group design. In-vitro culture of P. falciparum Papua 2300 strain were divided into a control group (K) and treatment groups that were treated regularly with artemisinin, i.e. artemisinin exposure I (PO1), artemisinin exposure 2 (PO2) and artemisinin exposure 3 (PO3) using IC50 concentration. The Tryptophan-rich Protein gene expression level was detected using qRTPCR. The result showed that in vitro repeated artemisinin exposure in P. falciparum Papua 2300 strain relatively increased the expression level of the Tryptophan-rich Protein (PArt) genes (2ΔΔCT) when comparedwith control. In conclusion, in vitro artemisinin exposure may cause Tryptophan-rich Proteins (PArt) gene overexpression by P. falciparum Papua 2300 strain promoter.

Keywords

• Artemisinin
• phenotype
• Triptophan-rich Protein (PArt) gene
• P. falciparum Papua 2300