Glucocorticoids — a hormone released into the blood by the adrenal glands — are essential for survival, but prolonged exposure to high concentrations of glucocorticoids — for example during chronic stress — can cause harm The results, especially for nerve cells. American scientists have now discovered that glucocorticoids can directly affect the mitochondrial function in nerve cells, thus revealing a mechanism by which these hormones can affect the function and survival of nerve cells.
Researchers such as Jing Du from the National Institutes of Health (NIH) tested the effects of the glucocorticoid adrenaline on the physiology (low concentration) and pathophysiology (high concentration) of mitochondrial function in cortical nerve cells in vitro. Both long-term and short-term treatment with low-dose epinephrine can increase mitochondrial oxidation levels (assessed with a dye that is sensitive to redox reactions), increase mitochondrial membrane potential (measured with a cationic dye), and increase mitochondrial Ca2 + Retention capacity (measured by coloration of a Ca2 + indicator). However, although short-term treatment of high-concentration adrenaline can produce similar effects, exposure to high-concentration adrenaline for 3 days can weaken all three mitochondrial function test results.
Adrenaline has a similar two-way effect on the survival of nerve cells. The researchers first treated nerve cells with high or low doses of adrenaline, and then reacted with kainic acid, which can cause apoptosis. The results showed that treatment with low-dose epinephrine for 1 or 3 days can enhance the survival probability of nerve cells; in these two periods of time, treatment with high-dose epinephrine worsens the apoptosis / effect of kainic acid.
The researchers then tested whether these effects were related to the translocation of glucocorticoid receptors (GRs) from the cytosol to the mitochondria. In fact, short-term (1.5 hours) treatment with low-dose or high-dose epinephrine can enhance the mitochondrial localization of GRs. However, after treatment with high-dose epinephrine for 3 consecutive days, the chance of this type of chromosomal translocation was reduced, while low-dose epinephrine did not cause this. The immunoprecipitation test further demonstrates this relationship. In mitochondria, GRs are combined with the anti-apoptosis / protein BCL2. Short-term exposure to high-dose and low-dose epinephrine increased the concentration of BCL2 in the mitochondria, but exposure to high-dose epinephrine for 3 consecutive days decreased the BCL2 concentration. Finally, experiments in living organisms also confirmed this finding-in laboratory mice, chronic treatment of adrenaline (3 weeks) reduced GR and BCL2 levels in the prefrontal cortex mitochondria of the brain. The researchers reported this research in the recently published Proceedings of the National Academy of Sciences.
In general, the researchers pointed out that physiologically low glucocorticoid levels can improve mitochondrial function, but high glucocorticoid levels will eventually weaken this function. This bidirectional effect of glucocorticoids is similar to the inverted U-shaped relationship between glucocorticoid levels and hippocampal toe function. This finding indicates that there is a mechanism that chronic stress is detrimental to the function and survival of nerve cells. Considering that virtually all cells contain mitochondria and GRs, it also affects other types of cells.
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