Throat spray formulated with virucidal Pharmaceutical excipients as an effective early prophylactic or treatment strategy against pharyngitis post-exposure to SARS CoV-2
In Silico, In Vitro, and rat study showing potential prophylactic and therapeutic benefits of a curcumin-loaded self-nanoemulsifying drug delivery system throat spray against SARS-CoV-2 infection and pharyngitis. Molecular docking studies identified DEAE-Dx, curcumin, trans-anethole, Tween 80, and PEG400 as top candidates for the spray formulation, based on binding to SARS-CoV-2 spike and main protease (Mpro) targets. The optimal formula, containing 0.1% curcumin, demonstrated anti-SARS-CoV-2 activity in vitro. In a rat model of acute pharyngitis, post-treatment with the curcumin spray significantly reduced proinflammatory markers TNF-α, IL-6, MCP-1, and IL-8. Preclinical toxicity tests in male rats confirmed the safety of the throat spray at a 5 µg/mL curcumin dose.
47 preclinical studies support the efficacy of curcumin for COVID-19:
In Silico studies predict inhibition of SARS-CoV-2 with curcumin or metabolites via binding to the spikeA,5,10,12,18,21 (and specifically the receptor binding domainB,8,11,14), MproC,5,7,9-11,13,14,16,19,21,22,24,37, RNA-dependent RNA polymeraseD,11,20, ACE2E,12,13,15, nucleocapsidF,6,23, nsp10G,23, and helicaseH,27 proteins.
In Vitro studies demonstrate inhibition of the spikeA,32 (and specifically the receptor binding domainB,40), MproC,17,32,37,39, ACE2E,40, and TMPRSS2I,40 proteins, and inhibition of spike-ACE2 interactionJ,25.
In Vitro studies demonstrate efficacy in Calu-3K,38, A549L,32, 293TM,1, HEK293-hACE2N,17,30, 293T/hACE2/TMPRSS2O,31, Vero E6P,7,11,21,30,32-34,36,38, and SH-SY5YQ,29 cells.
Curcumin is predicted to inhibit the interaction between the SARS-CoV-2 spike protein receptor binding domain and the human ACE2 receptor for the delta and omicron variants8, decreases pro-inflammatory cytokines induced by SARS-CoV-2 in peripheral blood mononuclear cells36, alleviates SARS-CoV-2 spike protein-induced mitochondrial membrane damage and oxidative stress1, and may limit COVID-19 induced cardiac damage by inhibiting the NF-κB signaling pathway which mediates the profibrotic effects of the SARS-CoV-2 spike protein on cardiac fibroblasts41.
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