β-glucogallin from (Muntingia calabura L.) as glaucoma inhibitor: an in silico study

Glaucoma causes permanent vision loss by damaging the optic nerve and retinal ganglion cells, increasing intraocular pressure, and involving toxic inflammatory factors that contribute to cell death and disease progression. Owing to the frequent adverse effects of current medicines, safer alternatives are required. Cherry fruit (Muntingia calabura L.) contains β-glucogallin, which has antioxidant and anti-inflammatory properties; however, the potential of β-glucogallin as a neurodegenerative inhibitor in glaucoma has not been thoroughly examined in in silico studies. The potential of β-glucogallin in inhibiting the signaling pathway of TNFR1, matrix metalloproteinase 9 (MMP9), and endothelin receptor B (ETRB) linked to neurodegenerative illnesses in glaucoma is investigated in this work. The Protein Data Bank database provided ETRB, TNFR1, and MMP9, whereas the PubChem database provided the β-glucogallin. PyRx was used for molecular docking, which was visualized using PyMOL and Biovia Discovery Studio. YASARA software was used for molecular dynamics simulations. According to the molecular prediction, β-glucogallin and drug control of ETRB, TNFR1, and MMP9 had comparable interactions and equivalent binding affinities. Residues of Asn158 and Trp336 were identified in the interaction between β-glucogallin and the drug control on ETRB, Ser74, Arg77, and Lys75 in the interaction on TNFR1, Val145, and Pro146 in the interaction on MMP9. According to the RMSD backbone, number of hydrogen bonds, and RMSF value, the protein was stable and the interaction between β-glucogallin and TNFR-1 and MMP9 was stable; these results demonstrate the potential of β-glucogallins from Muntingia calabura L. as neurodegenerative glaucoma inhibitors.