Molecular Docking of Cathelicidin (LL-37) in Mesenchymal Stem Cells Metabolite to Growth Factor, Antibacterial and Inflammatory Cytokine Biomarkers

Salivary gland function impairment is one example of a Type 2 Diabetes Mellitus (T2DM) consequence caused by a loss of microcirculation. Mesenchymal stem cells’ (MSCs) metabolite may modulate the immune response and fight pathogen infection through the synthesis of cathelicidin (LL-37) for tissue regeneration. Objectives to investigate the active compound of the MSCs’ metabolite, namely cathelicidin (LL-37), which binds to the effects of interleukin (IL)-10, IL-17, vascular endothelial growth factor (VEGF), fibroblast growth factor-2 (FGF-2), tumor growth factor beta (TGFβ), insulin growth factor (IGF), platelet-derived growth factor (PDGF), epidermal growth factor (EGF), hepatocyte growth factor (HGF), tissue inhibitor matrix metalloproteinase-1 (TIMP-1), matrix metalloproteinase (MMP)- 8 and -9, dectin, flaggelin, and peptidoglycan through a bioinformatics approach, in silico study. RCSB PDB was used to prepare the peptide Cathelicidin (LL37) (RCSB ID: 2K6O) and the biomarker targets for IL-10, VEGF, FGF2, IGF, HGF, EGF, TGFβ, PDGF, TIMP-1, Dectin, Flagelin, Peptidoglycan, IL-17, MMP-9, and MMP-8. PyMol v2.5 software for molecular docking optimization and standard publication-style visualization was used to remove water molecules and ligand impurities from target surfaces. Cathelicidin (LL-37) has a great negative binding energy value with IL-10, VEGF, FGF2, IGF, HGF, EGF, TGFβ, PDGF, TIMP1, Dectin, Flagelin, Peptidoglycan, IL-17, MMP-9, and MMP-8. Cathelicidins (LL-37) in MSC’s metabolite has high negative binding energy value that may inhibits pro-inflammatory cytokines, microbial, tissue degradation enzyme related biomarkers and increase anti-inflammatory cytokines and growth factor as documented in silico.