Network Pharmacology Analysis of Traditional Chinese Medicine Formula Shuang Di Shou Zhen Tablets Treating Nonexudative Age-Related Macular Degeneration

Abstract

Objective To analyze the pharmacological mechanism of the treatment of dry age-related macular degeneration (dry AMD) based on a network pharmacological approach of Shuang Di Shou Zhen Tablets (SDSZT) and to provide a new reference for the current lack of effective treatment of dry AMD. Methods The main chemical constituents and their targets of Rehmanniae Radix Praeparata, Ligustrum lucidum, Mori Fructus, Paeonia albiflora, Rhizoma Dioscoreae, Alisma orientale, Schisandra chinensis, Radix Polygoni Multiflori Preparata, Ophiopogon japonicus, and Radix Rehmanniae were obtained from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) and Traditional Chinese Medicine Integrated Database (TCMID). The active ingredients of traditional Chinese medicine were screened according to Absorption, Distribution, Metabolism, and Excretion (ADME), the gene names of the targets of each active ingredient were obtained from the Uniprot database, the main targets of dry AMD were obtained from GeneCards and DisGeNET database, and the protein interaction analysis was performed on the String database. The Metascape database was used to analyze the “drug-component-target” and the biological processes and networks involved, and then, Cytoscape 3.8.1 was used to construct the “ SDSZT component-dry AMD target-pathway” network. Results The main active ingredients of SDSZT for dry AMD treatment are quercetin, kaempferol, luteolin, β-glutamine, β-carotene, etc. And, the core targets are RAC-alpha serine/threonine-protein kinase (AKT1), prostaglandin G/H synthase 1 (PTGS1), tumor necrosis factor (TNF), transcription factor AP-1 (JUN), apoptosis regulator Bcl-2 (BCL2), caspase-3 (CASP3), phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit gamma isoform (PIK3CG), androgen receptor (AR), apoptosis regulator BAX (BAX), etc. The biological pathways for the treatment of age-related macular degeneration by SDSZT mainly act on pathways in cancer, fluid shear stress and atherosclerosis, and TNF signaling pathway, and the main function of SDSZT is to regulate intracellular cytokine receptor binding. Conclusion This study initially reveals the multiconstituent, multitarget, and multipathway mechanism of action of SDSZT in the treatment of dry AMD and provides the basis for the clinical application of SDSZT.