Why do we age?
According to the latest statistics released by the World Health Organization, the overall life expectancy of the Chinese population in 2020 has reached 77.3 years. While prolonging life, each of us hopes to be able to grow old healthily and avoid the debilitating and various diseases brought by old age. However, aging is a very complicated problem. In addition to age, there are many factors that cause aging.
A study published in the latest issue of Science gives us a new understanding of the occurrence of aging: some immune cells may play an important role in accelerating aging.
A Spanish research team has proved through experiments in mice that when the metabolic capacity of T lymphocytes changes, the accumulated inflammation in the body will cause the animals to prematurely aging, and various "senile diseases" appear. Regulating the metabolic capacity of these immune cells or preventing inflammation caused by them is expected to allow us to delay aging and treat aging-related diseases. T cells are generally believed to play a protective role in the body against the invasion of pathogens such as bacteria and viruses, and actively remove damaged and dead cells. T cells become less resistant to pathogens as they age, which is why older people are more susceptible to infection and less responsive to vaccines. One reason for the weakening of T cells is that, like many other tissues, as they get older, the cells inside, which act as a power plant component, the mitochondria, will start to fail.
However, the changes in T cells may not only be a manifestation of aging, but also a promoter of it. To test this hypothesis, the researchers genetically engineered mouse T cells to lack a protein that works in the mitochondria, forcing them to metabolize energy in a less efficient way. When these mice grow up to 7 months old, for the mice, it was originally a nice age, but they are already old, and their physical condition is actually similar to 22 months old! A thorough examination of the mice showed that their heart, brain and lungs, and other systems exhibited a typical "disease co-existence," similar to what is known as "senile disease" in humans.
Specifically, the hearts of these mice atrophied, heart failure; Signs of neurological dysfunction, such as impaired motor coordination; The muscles atrophy weak, the body fat also substantial loss, becomes emaciated; They were also less resistant to foreign viruses than the control mice of the same age.
In addition, blood test results showed that cells immunized with these mice produced a large amount of cytokines that caused inflammation such as IL-6, IFN-g and TNF-a at levels comparable to normal 22-month-old mice, leaving them in a state of chronic inflammation. Researchers believe that early entry into inflammaging may be an important reason for the deterioration of the animal's physical condition.
Regarding IL-6、IFN-γ、TNF-α mentioned above, Right now, DLdevelop has developed several kinds of ELISA Kits, if you want to know more about these kits, you can visit our website:
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A study published in the latest issue of Science gives us a new understanding of the occurrence of aging: some immune cells may play an important role in accelerating aging.
A Spanish research team has proved through experiments in mice that when the metabolic capacity of T lymphocytes changes, the accumulated inflammation in the body will cause the animals to prematurely aging, and various "senile diseases" appear. Regulating the metabolic capacity of these immune cells or preventing inflammation caused by them is expected to allow us to delay aging and treat aging-related diseases. T cells are generally believed to play a protective role in the body against the invasion of pathogens such as bacteria and viruses, and actively remove damaged and dead cells. T cells become less resistant to pathogens as they age, which is why older people are more susceptible to infection and less responsive to vaccines. One reason for the weakening of T cells is that, like many other tissues, as they get older, the cells inside, which act as a power plant component, the mitochondria, will start to fail.
However, the changes in T cells may not only be a manifestation of aging, but also a promoter of it. To test this hypothesis, the researchers genetically engineered mouse T cells to lack a protein that works in the mitochondria, forcing them to metabolize energy in a less efficient way. When these mice grow up to 7 months old, for the mice, it was originally a nice age, but they are already old, and their physical condition is actually similar to 22 months old! A thorough examination of the mice showed that their heart, brain and lungs, and other systems exhibited a typical "disease co-existence," similar to what is known as "senile disease" in humans.
Specifically, the hearts of these mice atrophied, heart failure; Signs of neurological dysfunction, such as impaired motor coordination; The muscles atrophy weak, the body fat also substantial loss, becomes emaciated; They were also less resistant to foreign viruses than the control mice of the same age.
In addition, blood test results showed that cells immunized with these mice produced a large amount of cytokines that caused inflammation such as IL-6, IFN-g and TNF-a at levels comparable to normal 22-month-old mice, leaving them in a state of chronic inflammation. Researchers believe that early entry into inflammaging may be an important reason for the deterioration of the animal's physical condition.
Regarding IL-6、IFN-γ、TNF-α mentioned above, Right now, DLdevelop has developed several kinds of ELISA Kits, if you want to know more about these kits, you can visit our website:
https://dldevelop.com/Research-reagent/dl-il6-mu.html
https://dldevelop.com/Research-reagent/dl-ifng-mu.html
https://dldevelop.com/Research-reagent/dl-tnfa-mu.html
