Anti-inflammatory “switch” could stop chronic inflammation and reverse aging
While inflammation is the body’s natural defense against threats, prolonged inflammation may lead to diseases like Alzheimer’s, Parkinson’s, cancer, multiple sclerosis (MS), and Type-2 diabetes. However, a molecular “switch” could essentially turn off unnecessary inflammation, potentially reversing these conditions and,maybe, even aging itself, according to researchers at the University of California, Berkeley (UC Berkeley), US.
They found a way to turn off the NLRP3 inflammasome – a group of immune proteins that launches an inflammatory response to fight off infections and so on. Specifically, the researchers found that a protein called SIRT2 acted as the switch in a “deacetylation” process, where a fragment of molecular matter is removed.
Danica Chen, Associate Professor of metabolic biology, nutritional sciences, and toxicology at UC Berkeley, explains, “This acetylation can serve as a switch – when it is acetylated, this inflammasome is on. When it is deacetylated, the inflammasome is off.”
In engineered mice that were unable to produce SIRT2, the researchers found that the animals showed more signs of inflammation and higher insulin resistance. Then, in groups of older mice that had their immune systems “rebooted” to have either the acetylated or deacetylated versions of the NLRP3 inflammasome, the researchers found that the deacetylated mice, overall, had better insulin resistance.
The findings suggest that drugs that are able to switch off NLRP3 could help treat conditions associated with inflammation, including the diseases mentioned above. These kinds of drugs could be used to reverse aging itself.
“My lab is very interested in understanding the reversibility of aging,” says Chen. “Now, we are asking: to what extent can aging be reversed? And we are doing that by looking at physiological conditions, like inflammation and insulin resistance, that have been associated with aging-related degeneration and diseases.”
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