<![CDATA[Plasmodium resisten terhadap artemisinin menjadi salah satu permasalahan kesehatan di dunia karena belum ada obat baru pengganti artemisinin. Resistensi P. falciparum terhadap obat antimalaria artemisinin dapat terjadi karena dipengaruhi oleh faktor internal dari P. falciparum, antara lain induksi ekspresi gen yang mengekspresikan protein. Salah satu gen tersebut adalah gen Triptophan-rich Protein (PArt). Fungsi Triptophan-rich Protein penting dalam membrane-spanning protein dan berperan dalam folding protein untuk menjaga kontak hidrofobik. Penelitian ini bertujuan membuktikan overekspresi gen Triptophan-rich Protein P. falciparum galur Papua 2300 yang disebabkan oleh paparan artemisinin berulang in vitro. Waktu penelitian dilaksanakan bulan Februari sampai November 2013. Tempat penelitian di Rumah Sakit Penyakit Tropik dan Infeksi Universitas Airlangga. Desain penelitian yang digunakan adalah experimental design dengan post test only control group design. Kultur in vitro P. falciparum galur Papua 2300 dibagi dalam kelompok kontrol (K) dan kelompok perlakuan paparan artemisinin berulang, yaitu paparan artemisinin ke-1 (PO1), paparan artemisinin ke-2 (PO2) dan paparan artemisinin ke-3 (PO3) menggunakan konsentrasi IC50. Ekspresi gen Triptophan-rich Protein (PArt) diukur dengan qRTPCR. Hasil menunjukkan paparan artemisinin berulang pada P. falciparum dapat meningkatkan level ekspresi gen Part (2??CT) relatif terhadap kontrol. Simpulan, paparan artemisinin in vitro menyebabkan overekspresi gen Tryptophan-rich Proteins(PArt) oleh promoter P. falciparum galur Papua 2300. [MKB. 2015;47(3):129?36]Kata kunci: Artemisinin, fenotip, gen Triptophan-rich Protein (PArt), P. falciparum galur Papua 2300 Effect of Artemisinin Exposure toward PArt Gene Expression in Plasmodium falciparum Papua 2300 StrainAbstract Artemisinin resistant Plasmodium has become one of the worldwide health problems, since there is currently 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 (2??CT) when comparedwith control. In conclusion, in vitro artemisinin exposure may cause Tryptophan-rich Proteins (PArt) gene overexpression by P. falciparum Papua 2300 strain promoter. [MKB. 2015;47(3):129?36]Key words: Artemisinin, phenotype, Triptophan-rich Protein (PArt) gene, P. falciparum Papua 2300 DOI: 10.15395/mkb.v47n3.593 ]]>
