A new study published in the journal Cell Metabolism by the team at the University of California, Berkeley, suggests they have found a “molecular switch” that controls the immune mechanism of chronic inflammation in the body or may lead to new ways to stop or even reverse many age-related diseases,media reported.
In the study, Danica Chen of the University of California, Berkeley, and her team showed that overactivation of the immune protein NLRP3 inflammatory small body was associated with a variety of chronic diseases, including multiple sclerosis, cancer, diabetes and dementia. The acetylation reaction or shutdown of the drug against this NLRP3 inflammatory small body may help prevent or treat these diseases.
By studying macrophages in mice, an immune cell, the team found a protein called SIRT2 responsible for the acetylation response of the NLRP3 inflammatory small body. Two-year-old mice bred to block the production of the SIRT2 protein showed more signs of inflammation than normal mice. The mice also showed higher insulin resistance, a disease associated with type 2 diabetes and metabolic syndrome.
The team also studied older mice whose immune systems were compromised and then produced an NLRP3 inflammatory small body with acetylation reactions from hematopoietic stem cells. It was found that mice with inflammatory microscoels, either with a biotylide reaction or “closed” form, improved insulin resistance after six weeks, suggesting that turning off this immune mechanism may reverse the process of metabolic disease.
‘I think this finding is very important for treating major chronic diseases in humans, ‘ the researchers said, ‘because many promising Alzheimer’s trials have failed.’ Therefore, it is more important to urgently understand the reversibility of aging-related diseases and to use this knowledge to help develop drugs to treat aging-related diseases.