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Older people are more susceptible to viral infections than younger people and experience higher mortality rates from the virus. Defects in the way our cells fight viruses may exacerbate the problem, because viruses require energy. Because nicotinamide adenine dinucleotide (NAD+) boosts energy production but decreases with age, scientists at SBX Biosciences in Japan studied the effects of boosting NAD+ on cellular antiviral defenses.
In Scientific Reports , Sano and colleagues show that NMN blocks the activation of a pro-inflammatory protein called IL-6 in artificially infected human cells. Additionally, they showed that NMM reduced activation of a protein called PARP9, suggesting victory on the so-called "NAD+ battlefield," in which PARP9 has sufficient levels of NAD+ to overcome viral proteins. These findings suggest that NMN can reduce virus-mediated inflammation and help protect against viruses.
To simulate a viral infection, Sarno and colleagues exposed human lung cells to a synthetic chemical called polyinosinic acid (PPA), which mimics a viral infection. The researchers then treated PPA-infected human cells with low (0.1 mM), medium (1.0 mM), or high (10.0 mM) doses of NMN, which is known to replenish cellular NAD+ levels.
Generally speaking, genetic information flows in one direction, from DNA to messenger RNA (mRNA) to protein. Typically, this mRNA is measured to estimate the production of its corresponding protein. It follows that since we already know the function of most proteins, we can predict how cells will function based on changes in mRNA levels.
Sano and colleagues found that mRNA levels of interleukin-6 (IL-6), a pro-inflammatory protein, were elevated in infected human lung cells, indicating increased inflammation. However, IL-6 mRNA decreased to normal levels after treatment with high-dose NMN. These findings suggest that NMN can reduce virus-mediated inflammation.
The "NAD+ battlefield" involves a battle between the human protein PARP and proteins produced by viruses. The NAD+ battlefield is so named because NAD+ is broken down by PARP, which cleaves the ADP-ribose molecule from the NAD+ molecule. PARP then attaches the ADP ribose molecule to the protein. The viral protein does the opposite, removing the ADP-ribose molecule from the protein. Since the addition of ADP-ribose to specific proteins can destroy viruses, it is crucial for PARP to win this battle.
The mRNA levels of PARP9, a specialized form of PARP, were found to be elevated in infected cells. However, high doses of NMN reduced PARP9 mRNA levels, indicating that high PARP levels are no longer required. These findings suggest that NMN helps win on the NAD+ battlefield by increasing NAD+ levels.
A key property of NMN is its ability to suppress inflammation. Chronic inflammation causes damage to organs and tissues and is at the root of many age-related diseases. Therefore, by reducing inflammation, NMN also combats one of the main underlying features of many diseases.
NMN has been shown to reduce pro-inflammatory proteins secreted by immune cells during hypersensitivity reactions in mice. NMN has also been shown to reduce pro-inflammatory factors in the gut, thereby treating inflammatory bowel disease and reducing obesity-related inflammation in adipose tissue. Pro-inflammatory proteins including IL-6 have also been shown to be reduced in response to NMN in lung injury. Recently, NMN was shown to reduce brain inflammation—an overactive immune response that leads to systemic inflammation—in a mouse model of sepsis. Therefore, NMN can reduce a variety of age-related inflammations, supporting its role as an anti-inflammatory and anti-aging compound.
*Special note - This article is for informational purposes only and cannot replace a doctor's treatment diagnosis and advice. It should not be regarded as a recommendation or proof of efficacy of the medical products involved. If it involves disease diagnosis, treatment, and rehabilitation, please be sure to go to a professional medical institution to seek professional advice.
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