Can things in broccoli and Brussels sprouts prevent COVID-19?
Can things in broccoli and Brussels sprouts prevent COVID-19?

Can things in broccoli and Brussels sprouts prevent COVID-19?

A chemical derived from a compound found in broccoli and other cruciferous plants may offer a potentially new and potent weapon against the viruses that cause COVID-19 and the common cold, new evidence suggests.

COVID-19 has already killed more than 6 million people worldwide, and studies have shown that the common cold costs an estimated economic loss of $ 25 billion in the United States alone each year.

In the study in the journal Communication Biologyit showed scientists sulforaphanea plant-derived chemical, known as a phytochemical, which has already been shown to have anti-cancer effects, may inhibit the replication of SARS-CoV-2, the coronavirus that causes COVID-19, and another human coronavirus in cells and mice.

While the results are promising, the researchers warn the public against rushing to buy sulforaphane supplements available online and in stores, noting that studies on sulforaphane in humans are needed before the chemical is proven effective, and stressing the lack of regulation, covering such supplements.

The natural precursor of sulforaphane is particularly abundant in broccoli, cabbage, kale and Brussels sprouts. First identified as a “chemo-preventive” compound decades ago, natural sulforaphane is derived from common food sources, such as broccoli seeds, sprouts and ripe plants, as well as infusions of sprouts or seeds for drinking.

Previous studies, including those at Johns Hopkins Medicine, have shown that sulforaphane has cancer and infection-preventing properties by disrupting certain cellular processes.

“When the COVID-19 pandemic started, our interdisciplinary research team changed our studies of other viruses and bacteria to focus on a potential treatment for what was then a challenging new virus for us,” says senior author Lori Jones-Brando, an assistant professor pediatrics at Johns Hopkins University School of Medicine.

“I screened several drugs for anti-coronavirus activity and decided to try sulforaphane as it has shown modest activity against other microbial agents that we are studying. “The researchers used purified, synthetic sulforaphane purchased from commercial chemical suppliers in their experiments.

In one experiment, the research team first exposed cells to sulforaphane for one to two hours before infecting the cells with SARS-CoV-2 and the common cold coronavirus, HCoV-OC43. They found that low micromolar (µM) concentrations of sulforaphane (2.4-31 µM) reduced replication by 50% of six strains of SARS-CoV-2, including the Delta and Omicron variants, as well as of HCoV- OC43 coronavirus. The researchers also observed similar results with cells that had previously been infected with viruses, where the protective effects of sulforaphane were seen even with an already established viral infection.

The group also studied the effects of sulforaphane in combination with remdesivir, an antiviral drug used to shorten the healing of hospitalized adults with COVID-19 infections.

They found out remdesivir inhibited 50% of the replication of HCoV-OC43 and SARS-CoV-2 at 22 µM and 4 µM, respectively. In addition, the research team reports that sulforaphane and remdesivir interacted synergistically at several combination conditions to reduce the viral load in cells infected with HCoV-OC43 or SARS-CoV-2 by 50%.

In this context, synergism means that lower doses of both sulforaphane (eg 1.6-3.2 µM) and remdesivir (eg 0.5-3.2 µM) when combined are more effective against viruses than individually.

“Historically, we have learned that the combination of several compounds in a treatment regimen is an ideal strategy for treating viral infections,” said Alvaro Ordonez, first author of the paper and an assistant professor of pediatrics. “The fact that sulforaphane and remdesivir work better combined than alone is very encouraging.”

The researchers then performed studies in a mouse model of SARS-CoV-2 infection. They found that giving 30 milligrams of sulforaphane per kilograms of body weight to mice before being infected with the virus significantly reduced the loss of body weight typically associated with viral infection (7.5% decrease).

Furthermore, the pretreatment resulted in a statistically significant decrease in both the amount of virus or the amount of virus in the lungs (17% decrease) and upper respiratory tract (9% decrease) as well as the amount of lung damage (29% decrease)) compared to infected mice that did not get sulforaphane. The compound also reduced inflammation in the lungs and protected the cells from a hyperactive immune response that appears to be one of the driving factors that has caused many people to die from COVID-19.

“What we found is that sulforaphane is antiviral to HCoV-OC43 and SARS-CoV-2 coronavirus, while also helping to control the immune response,” says Ordonez. “This multifunctional activity makes it an interesting compound to use against these viral infections as well as those caused by other human coronaviruses.”

The team plans to conduct studies on humans to assess whether sulforaphane may be effective in preventing or treating these infections.

“Despite the introduction of vaccines and other drugs that may have side effects, effective antiviral drugs are still needed to prevent and treat COVID-19, especially given the potential effects of new coronavirus variants occurring in the population. , “says Jones-Brando. “Sulforaphane could be a promising treatment that is cheaper, safer and more readily available commercially.”

Additional co-authors are from Johns Hopkins. The National Institutes of Health, Mercatus Center, Center for Infection and Inflammation Imaging Research at Johns Hopkins University School of Medicine and the Stanley Medical Research Institute funded the work.

Jones-Brando, Ordonez, and co-authors Robert H. Yolken and Sanjay K. Jain are co-inventors of a pending patent application filed by Johns Hopkins University. All other authors have no competing interests.

Source: Johns Hopkins University

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