There are several studies evaluating the clinical benefit of quercetin Australia. These include nine phase-2 clinical trials that evaluated quercetin vs. COVID-19. According to the National Institutes of Health database, four were completed while the results from one were published in a peer-reviewed journal. Although the results of these studies were preliminary, they do provide some insight into the potential benefits of quercetin in COVID 19.
Quercetin inhibits NLRP3 inflammasome activation
One of the most important aspects of COVID-induced inflammation is cytokine production. When these molecules are too abundant, they can trigger a cytokine storm. As a result, severe COVID-induced inflammation and oxidant/antioxidant imbalance can occur. Quercetin inhibits NLRP3 inflammasome activation by impairing the formation of oligomerization of the ASC. This means that quercetin prevents the production of IL-1b and IL-18.
In addition, quercetin enhances IL-10 and HO-1 expressions, and inhibits NLRP3 inflammasomal activity. These effects suggest that quercetin is a promising treatment for severe COVID-induced inflammation. Fig. 1 highlights the key Molecular Mechanisms of quercetin's action.
It reduces permeability of the intestinal microbiome.
Several studies have demonstrated the beneficial effects of certain prebiotics and probiotics on gut permeability. For example, lactobacillus rhamnosus and Faecalibacterium prausnitzii can significantly reduce intestinal permeability. Similarly, E. Coli strain Nissle 1917 is capable of reducing permeability. Interestingly, both prebiotics and probiotics can also increase zonulin levels.
Intestinal permeability has been linked to an increased number of circulating endotoxins. Increased intestinal permeability promotes exposition to luminal contents by inflammatory bowel disease, Crohn's disease, and ulcerative colitis. This, in turn, activates the immune response. In addition, intestinal permeability has been linked to altered mucosal barrier function. This alteration may represent primary dysfunction in patients with ulcerative colitis and Crohn's disease. These alterations may also perpetuate chronic mucosal inflammation in the latter.
It inhibits inflammatory factor secretion.
One of the mechanisms that explains the clinical deterioration of COVID-19 patients is the cytokine storm, a cascade of events triggered by invading viruses or bacteria. Inflammatory cytokines like interleukin-1 (IL-1) are released due to this cascade of events. As a result, these patients are infected with high-risk diseases, according to the study.
However, because of the high risk of infection in COVID-19 patients, several treatment options have been introduced recently to reduce the cytokine storm and treat severe illness. In the meantime, ongoing research examines novel cytokine blockade therapies and traditional anti-inflammatory drugs. These treatment options will likely help to improve patient's quality of life and minimize future hospitalizations.
It maintains liver function.
The mechanisms of action of quercetin are complex and overlap with the pathophysiology of COVID-19. For example, the research from Pierce et al. and Bindoli et al. shows that quercetin modulates the expression of 98 human genes that encode SARS-CoV-2 protein targets. In addition, quercetin inhibits 23 of 27 viral proteins.
There is a vast amount of scientific literature on quercetin. Among other things, quercetin has antiviral, antioxidant, anti-inflammatory, and immunomodulating properties. It has also been shown to inhibit specific key proteins in COVID-19. In addition, Riva and colleagues have demonstrated positive effects in patients treated with quercetin. But further research must be done to prove that quercetin is beneficial for COVID-19 prophylaxis.
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