Galangin for COVID-19 and Mucormycosis co-infection: a potential therapeutic strategy of targeting critical host signal pathways triggered by SARS-CoV-2 and Mucormycosis

Abstract

Mucormycosis co-infection with COVID-19 patients has a poor prognosis for fatality. However, they do not have any therapeutic choices right now. Galangin is prone to both COVID-19 and Mucormycosis, according to an ongoing study; galangin was investigated as a prospective molecular mechanism against COVID-19 with Mucormycosis co-infection to determine its functional role and underlying mechanisms of action. In SARS-COV-2 and Mucormycosis co-infection, we have conducted a series of computational approaches to identify and describe the beneficial mechanism, and pharmacological targets with therapeutic strategies of galangin against this type of co-infections. COVID-19 and Mucormycosis were characterized by pathological mechanisms, essential signaling pathways, and potential therapeutic intervention. Protein–protein interaction (PPI) was constructed for 57 common gene targets associated with co-infection. The pharmacological options were TNF (− 7.4 kcal/mol), CASP3 (− 7.3 kcal/mol), and MMP9 (− 7.7 kcal/mol) were proposed potential therapeutic targets validated through molecular docking and molecular dynamics simulation studies. Signaling pathways, molecular properties, and upstream pathway activity were also revealed in COVID-19 and Mucormycosis, along with galangin. However, treatment with galangin indicated that it could inhibit several cytokines, including TNF-α, TGF-β1, and IL-6 release which reduces inflammation and tissue injury through IL-17, HIF-1α, TGF-β, and cytokine-mediated signaling pathways. The most significant transcription factor (TF) E2F1 and miRNA hsa-miR-16-5p were identified through gene regulatory network analysis to serve as diagnostic biomarkers. However, galangin may be a possible therapeutic medication for the treatment of COVID-19 and Mucormycosis.