Exploring the potential of Beta- 2 Agonist, Salbutamol Against Muscle Atrophy Using Computational Approach

Abstract

Background: Muscle atrophy affects many individuals every year, and there are only a few FDA-approved drugs to treat skeletal
muscle wasting. This is caused by a combination of factors including inactivity, aging, and a wide range of diseases such as diabetes,
cancer, neurodegenerative disorders, bacterial and viral infections, chronic respiratory and renal diseases, and several drug side
effects.
Aim: Therefore, the present study was aimed to evaluate the anti-muscle atrophy potential of existing beta 2 agonist, salbutamol
through in silico approach.
Methods: Solubility analysis of salbutamol was performed in different solvents i.e. water, ethanol, ether, HCl, and chloroform to
confirm the solubility behaviour. Calibration curve of salbutamol was prepared in 0.1N HCl (276 nm) and assessed by UV
spectroscopy. Fourier transform infrared spectroscopy (FTIR) analysis of salbutamol was performed to confirm the purity of
salbutamol. Furthermore, molecular docking was performed using the Autodock Vina software to confirm the affinity of ligandprotein complexes (AKT1, Growth differentiation factor 8 (GDF-8), IGF-1, MuRF-1, MyoD, and TNF-α).
Results: Solubility results showed that salbutamol was sparingly soluble in water and ether, freely soluble in 0.1 N HCl solutions, and
also in ethanol and chloroform which indicates the drug is highly soluble. The calibration curve uses to assess the amount of drug in
plasma a different time interval. FTIR results of salbutamol showed sharp peaks at 4000-400 cm-1 wavelengths. The molecular
docking shows the high binding energy with the target protein viz. AKT1, Growth differentiation factor 8 (GDF-8), IGF-1,
MuRF-1, MyoD, and TNF
Conclusions: Results demonstrate that β2-adrenergic agonist salbutamol shows good binding affinity to catabolic (MuRF-1,
myostatin, MyoD and TNF-α) and anabolic proteins (AKT1, IGF-1, and GDF-8) through a computational approach to predict the
skeletal muscle atrophy.