In Silico and In Vitro study showing potential benefits of curcumin for severe COVID-19 by protecting mitochondrial function and reducing dysregulated metabolism and immune response. Authors identified five mitochondrial dysfunction biomarkers (RECQL4, PYCR1, PIF1, POLQ, GLDC) that distinguish severe COVID-19 patients and regulate abnormal metabolism and immunity. In Silico screening of 496 natural compounds found curcumin had the highest potential to modulate these biomarkers. In Vitro, pre-treatment with curcumin for 8 hours alleviated SARS-CoV-2 S1 protein-induced mitochondrial membrane potential damage and reduced elevated reactive oxygen species levels in cells.
46 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,5,7,9-11,13,14,16,19,21,22,24,36, RNA-dependent RNA polymeraseD,11,20, ACE2E,12,13,15, nucleocapsidF,6,23, nsp10G,23, and helicaseH,26 proteins.
In Vitro studies demonstrate inhibition of the spikeA,31 (and specifically the receptor binding domainB,39), MproC,17,31,36,38, ACE2E,39, and TMPRSS2I,39 proteins.
In Vitro studies demonstrate efficacy in Calu-3J,37, A549K,31, 293TL,1, HEK293-hACE2M,17,29, 293T/hACE2/TMPRSS2N,30, Vero E6O,7,11,21,29,31-33,35,37, and SH-SY5YP,28 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 cells35, 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 fibroblasts40.
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