In Vitro study showing that a water-dispersible nano-spray formulation of curcumin inhibits SARS-CoV-2 infection in Vero E6 cells. Authors found that pre-treatment effectively inhibited SARS-CoV-2 infection, and subsequent exposure to the nanoformulation after infection inhibited viral particle spread. There was no cytotoxicity at the tested concentrations on Vero E6 cells.
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.
4 studies investigate novel formulations of curcumin for improved efficacy11,28,42,43
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