Abstract
Atherosclerosis is a chronic inflammatory disease that begins with endothelial dysfunction, it caused fat accumulation and plaque growth in the inner arteries walls. Endothelial dysfunction will activate the Mitogen Activated Protein Kinase (MAPK) pathway involving ERK1, ERK2, JNK1, JNK2, and p38MAPK proteins, as well as the Nuclear Factor Kappa B (NF-kB) pathway involving IKK proteins. Terpinen-4-ol is constituent found in the bangle rhizome. The purpose of this study were to determine the affinity and mechanisms of terpinen-4-ol against ERK1, ERK2, JNK1, JNK2, and p38MAPK proteins as anti-inflammatory in atherosclerosis performed using molecular docking method. The study was conducted exploratively with several steps such as preparation and optimization of terpinen-4-ol structure, preparation of 3D ERK1, ERK2, JNK1, JNK2, and p38MAPK proteins, validation method of molecular docking, and docking terpinen-4-ol in these proteins. The docking result are assessed from the binding energy and hydrogen bonds formed between terpinen-4-ol and proteins. The smaller value of binding energy terpinen-4-ol with target proteins showed the complex that form more stable. The result showed that terpinen-4-ol and has activity in inhibiting the inflammatory process because it is able to disturb ERK1, ERK2, JNK1, JNK2, and p38MAPK proteins with respective bond energy values -5,12; -5,24; -5,08; -5,88; and -4,99 Kcal/mol. The molecular mechanism in inhibiting the activity of ERK1, ERK2, JNK1, JNK2, and p38MAPK proteins is through the formation of hydrogen bonds in these proteins. These results show that terpinen-4-ol have the potential to inhibit inflammatory process and the formation of atherosclerotic plaque can be obstructed.
 Keywords : atherosclerosis, terpinen-4-ol, molecular docking, in silico
Highlights
Atherosclerosis is a chronic inflammatory disease that begins with endothelial dysfunction, it caused fat accumulation and plaque growth in the inner arteries walls
These results show that terpinen-4-ol have the potential to inhibit inflammatory process and the formation of atherosclerotic plaque can be obstructed
Amino Acids (MAAs-Like) sebagai Senyawa Penyerap Sinar UV’, dipresentasikan pada Seminar Nasional Hasil Penelitian MIPA di Semarang, 4 Desember
Summary
Bahan yang digunakan yaitu struktur protein ERK1 (PDB ID : 4QTB), ERK2 (PDB ID : 4N0S), JNK1 (PDB ID : 3ELJ), JNK2 (PDB ID : 3NPC), dan p38MAPK (PDB ID : 1OUY) yang diunduh dari website protein data bank http://www.rcsb.org/pdb/home/home.do. serta struktur 3 dimensi terpinen-4-ol yang dibuat dan dipreparasi menggunakan program HyperChem 8. Serta struktur 3 dimensi terpinen-4-ol yang dibuat dan dipreparasi menggunakan program HyperChem 8. Alat yang digunakan dalam penelitian ini yaitu seperangkat komputer dengan spesifikasi Windows 7 (64 bit) dilengkapi program Hyperchem 8, Autodock 4.2, dan Chimera 1.10.1. Struktur tiga dimensi terpinen-4-ol dibuat dan dioptimasi menggunakan program HyperChem 8. Validasi Metode Molecular Docking Validitas metode molecular docking diketahui dengan cara men-docking-kan kembali native ligand pada protein target yang telah mengalami preparasi menggunakan program Autodock 4.2. Docking Terpinen-4-ol Pada Protein Target Terpinen-4-ol yang telah dioptimasi didocking-kan dengan protein target tanpa native ligand menggunakan program Autodock 4.2 dengan grid box hasil validasi. Molecular docking akan menghasilkan senyawa dengan konformasi tertentu yang memiliki energi ikatan paling rendah untuk berikatan dengan protein target. Mekanisme aktivitas senyawa uji dapat diketahui dari jenis interaksi (ikatan hidrogen) yang terbentuk antara terpinen-4-ol dengan protein target
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