@article {1865, title = {Potential Role of Mitragynine as Lipolysis Stimulator via Adrenergic Signalling: Docking Model Study}, journal = {Pharmacognosy Journal}, volume = {14}, year = {2022}, month = {October 2022}, pages = {527-531}, type = {Original Article}, chapter = {527}, abstract = {

Backgrounds: Mitragynine is the most popular of the more than 50 alkaloids contained in M.Speciosa. In particular, the Mitragynine alkaloid has the potential to increase lipid (fats) metabolism through specific pathways such as adenylyl cyclase signaling via adrenergic receptors. In this case, Asp Amino acid and Ser are the types of residues that can activate adenylyl cyclase to initiate a series of activities in cells. Methods: This study used Mitragynine ligand and adrenergic receptors (α1b, α2a, α2b, α2c dan β1). The receptor candidates were tested using Autodock whose test results were presented in the form of tables and 3-dimensional images using the Biovia Discovery Studio. Results: Hydrogen bonds were formed between Mitragynine and the amino acids Asp and Ser at the β1-adrenergic receptor. The binding amino acids were found in Ser20 and Asp21 with energy bond of -5.26 kcal/mol and IC50: 111.35 ppm. Meanwhile, at the adrenergic receptor α2b there was only Asp residue that formed hydrogen bond with Mitragynine namely Asp218A. The energy bond formed between the two was -5.19 kcal/mol and IC50: 125.04 ppm. Conclusion: Mitragynine has the potential to stimulate lipolysis through the pathways of α2b and β1-adrenergic receptors.

}, keywords = {Adrenergic, Docking, Lipolysis, Mitragynine}, doi = {10.5530/pj.2022.14.130}, author = {Khoirul Rista Abidin and Ronny Lesmana and Mas Rizky Anggun Adipurna Syamsunarno and Kelana Kusuma Dharma} } @article {1647, title = {The Potential Interaction of Ethionamide-Thyroid Hormone Receptor Induces Hypothyroidism}, journal = {Pharmacognosy Journal}, volume = {13}, year = {2021}, month = {September 2021}, pages = {1174-1179}, type = {Research Article}, chapter = {1174}, abstract = {

Background: Hypothyroidism is a common side effect found in patients with multidrug-resistant tuberculosis taking ethionamide. The mechanism of ethionamide-induced hypothyroidism is potentially caused by the structure of ethionamide compounds chemically similar to thioamide, such as propylthiouracil (C7H8N2S), which inhibits thyroid hormone synthesis. However, hypothyroidism is caused not only by a lack of production but also by signaling alteration. Thyroid hormone action is mediated by thyroid hormone receptors (TRs), members of the nuclear receptor superfamily that regulate their target genes. Unfortunately, there are limited studies on the potential interaction of ethionamide with TRs. Objective: In the present study, we want to elaborate on the potential interaction of ethionamide with TRs which might alter the thyroid hormone genomic regulation. Methods: Molecular docking studies were used to evaluate the potential interaction between ethionamide with TRα and TRβ. Results: The molecular docking results on TRα showed more than one hydrogen bond{\textendash}steric interaction formed from the ethionamide{\textendash}amino acid residue interaction. Ethionamide{\textendash}TRβ interaction showed more than one steric interaction, but the hydrogen bonds are not visualized. The docking score between ethionamide and TRα is -7.373 kcal/ mol and higher than its interaction with TRβ. Conclusion: These findings indicate that ethionamide can interact with TRα and TRβ. However, the ethionamide{\textendash}TRα interaction is stronger than ethionamide{\textendash}TRβ interaction. Our study reports a novel mechanism of action of ethionamide-induced hypothyroidism.

}, keywords = {Ethionamide, Hypothyroidism, Molecular docking, TRα, TRβ}, doi = {10.5530/pj.2021.13.150}, author = {Ronny Lesmana and Firyali Rahmani Shidqi and Hanna Goenawan and Iwan Setiawan and Marisca Evalina Gondokesumo and Farida Suhud and Nasrul Wathoni} }