Abstract

DLBS2411, a bioactive fraction of Cinnamomum burmannii, has been proven to exhibit its anti-ulcer properties through preclinical and clinical studies. However, the bioactive compounds, protein targets, and underlying molecular pathways are still poorly known. Therefore, network pharmacology was used in this study to understand the molecular mechanisms of DLBS2411 in treating gastritis. There were three stages in this investigation. First, the DLBS2411 compounds and targeted proteins associated with DLBS2411 and gastritis were gathered and examined. The subsequent stage involved constructing and analyzing the protein–protein interaction network. Then, molecular docking was employed to confirm the interaction between substances and proteins. This study found that most DLBS2411 compounds, including p-cymene, copaene, and cinnamaldehyde, were apparent in their effects on gastritis. These substances impacted several important target proteins, including PTGS1, PTGS2, 15-hydroxyprostaglandin dehydrogenase, NOS2, and ATPase H+/K+ transporting subunit alpha, which were associated with the mucosal protector and proton-pump inhibitor modes of action, consistent with earlier in vitro and in vivo studies. In addition, the molecular docking study revealed that the ligand-receptor binding activity had a good vina score, indicating stable ligand-protein complexes. Thus, it can be concluded that the proton pump inhibitor and mucosal protector were the key molecular pathways utilized by DLBS2411 to treat gastritis.

Key words: DLBS2411, Cinnamomum burmanii, gastritits, network pharmacology, molecular docking.