ArticleAdvances in experimental medicine and biology2026
Exploring Therapeutic and Multitarget Mechanism of Molsidomine on Cerebral Ischemia: Molecular Docking and Multifaceted In Silico Study.
Article in Advances in experimental medicine and biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The innate immune response is started immediately following brain ischemia, resulting in adaptive immunity. More and more experimental evidence has indicated that the immune response caused by cerebral ischemia plays a crucial role during the initial brain damage and subsequent brain injury recovery. Molsidomine, a nitric oxide donor, has been found to reduce schizophrenia-like behavioral abnormalities in rats due to glutamate hypofunction. The current study sought to explore the efficacy of molsidomine versus conventional drugs in cerebral ischemia. This study scavenges literature to retrieve various genes like PI3K, MMP9, COX2, LOX, TLR4, AKT1, mTOR, NLRP3, STAT3, IL1β, NFκB, TNF, IL6, and TP53 involved in cerebral ischemia. A two-step molecular docking revealed significant gene-drug complexes followed by a protein-protein interaction (PPI). Additionally, oncoprint analysis, protein-protein interaction, and functional and pathway enrichment associated with these genes and a circos plot depicting the mutational profile of the genes are incorporated in this study. This comprehensive in-silico approach reveals the efficacy of the potency of the candidate drug, molsidomine in treating cerebral ischemia.
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