In silico evaluation of natural opioid ligands interaction and their therapeutic prospects in neuroinflammation

利用计算机模拟评估天然阿片类配体相互作用及其在神经炎症中的治疗前景

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Abstract

Opioids are potent analgesics and sedative compounds that acts primarily through opioid receptor (ORs) as µOR, δOR, κOR. Beyond their well-established roles in pain management, mood regulation, respiratory control, and ionic homeostasis, opioids are increasingly recognized for their modulating neuroinflammation via receptor-mediated pathways influencing glial activity and inflammatory signaling. The present study aimed to comparatively evaluate the pharmacokinetic profile and receptor-binding affinities of five natural opioids including morphine, codeine, noscapine, papaverine, and thebaine with a focus on their therapeutic efficacy, safety profile, and molecular targets implicated in opioid-mediated neuroinflammation to identify promising candidates for effective therapeutic intervention. Through integrative computational approaches including molecular docking, ADMET analysis, and network pharmacology, the study revealed favourable absorption and distribution for all compounds, though, morphine, noscapine, and papaverine exhibited potential toxicity. Differences in metabolism and excretion suggested variable pharmacokinetics. GO and KEGG analyses revealed involvement in calcium channel activity, neurotransmitter regulation, and dopaminergic synapse signaling. Protein Protein Interaction (PPI) network highlighted DRD2, OPRM1, and SIGMAR1 as key hub genes. Molecular docking showed noscapine, papaverine, and morphine had the highest affinity for µOR; morphine, codeine, and thebaine for δOR; and noscapine, papaverine, and thebaine for κOR. OPRM1 emerged as the primary target, followed by SIGMAR1 and DRD2. MD simulation suggest receptor's structural stability, supporting their potential to engage DRD2 in biologically relevant conformational states. The comparative analysis underscores the distinct pharmacological profiles of natural opioids and identifies potential molecular targets for developing safer, neuroinflammation-focused opioid therapies. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s40203-026-00584-w.

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