Abstract
Skin aging caused by excessive exposure to ultraviolet is known as photoaging. The mechanism underlying skin photoaging relates to collagen degradation in the extracellular matrix (ECM) by overexpression of matrix metalloproteinases-1 (MMP-1). Gallic acid is a phenolic antioxidant found in many types of plants and can be used as an anti-photoaging agent due to its antioxidant activity. This study aims to determine the potential effect of gallic acid as an anti-photoaging against MMP-1 using in silico molecular docking. The stages included gallic acid structure optimization using the HyperChem 8, preparation of protein target MMP-1 (PDB ID: 966C) using the Chimera1.10.1, validation the molecular docking protocol, and docking gallic acid on MMP-1 with the Autodock 1.5.6. The results showed that gallic acid had an affinity for MMP-1 with a binding energy of -6.0 kcal/mol. There are similar amino acid residues in hydrogen bonds between the native ligand RS2 with MMP-1 and gallic acid with MMP-1, namely ALA 182, LEU 181, and HIS 218. The results suggest that gallic acid has the potential as the anti-photoaging agent through the inhibition of the MMP-1 enzyme.
Highlights
Aging is a physiological process that is caused by intrinsic and extrinsic factors
reactive oxygen species (ROS) inhibit the activity of receptor protein tyrosine phosphatases (RPTPs) by binding to cysteine at the catalytic site of RPTPs, increasing the level of phosphorylated receptor tyrosine kinases (RTKs) and triggering the activation of mitogen-activated protein kinase (MAPK), which in turn activates nuclear factor kappa-B (NF-κB) and transcription factor activator protein-1 (AP-1)
The matrix metalloproteinases-1 (MMP-1) protein was separated from RS2 native ligand to make the binding site available for the docking process of gallic acid
Summary
Aging is a physiological process that is caused by intrinsic and extrinsic factors. Intrinsic factors occur naturally with age, while extrinsic factors are associated with external exposure, such as ultraviolet light. Skin aging is caused by exposure to ultraviolet rays known as photoaging. Exposure to ultraviolet radiation causes the formation of reactive oxygen species (ROS) in the skin layer that triggers activator protein-1 (AP-1) activity. ROS inhibit the activity of receptor protein tyrosine phosphatases (RPTPs) by binding to cysteine at the catalytic site of RPTPs, increasing the level of phosphorylated receptor tyrosine kinases (RTKs) and triggering the activation of mitogen-activated protein kinase (MAPK), which in turn activates nuclear factor kappa-B (NF-κB) and transcription factor AP-1. Induction of AP-1 will activate matrix metalloproteinases (MMPs) [1,2]
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