Stroke can cause irreversible, life-altering, and long-term brain damage. A stroke can be caused by a blood clot called a thrombus. ischemic strokeor a ruptured blood vessel. hemorrhagic stroke. Our brains require large amounts of oxygen, so when blood flow is interrupted, oxygen-dependent brain substances are damaged in the short term.

Think of the blood vessels in your brain as a perfectly designed highway. When an ischemic stroke occurs, blood clots block these blood vessels, preventing oxygen from reaching the brain. When an ischemic stroke occurs, microglia It acts as our body's “ambulance” and focuses on the site of the blood clot. Scientists classify microglia into two types: anti-inflammatory and pro-inflammatory. Anti-inflammatory microglia help fight inflammation in the brain. Pro-inflammatory microglia cause further brain inflammation by damaging nerve cells. neuronremove the protective sheath known as . myelin.

Chinese researchers recently developed a hypothesis that inhibits an enzyme associated with inflammation called histone deacetylase 3 or HDAC3 may reduce proinflammatory microglial production in mice. They reasoned that because HDAC3 enzymes activate proinflammatory immune cells, inhibiting these enzymes may reduce inflammation.

To study how stroke affects the production of inflammatory cells, the researchers first determined which cell types in mice were most likely to be affected by HDAC3. They induced strokes in mice and found that HDAC3 was more active in the mice's microglia than in other cells. High levels of HDAC3 were present in the mice's neurons, but they were not active. The researchers interpreted this data to suggest that HDAC3 plays a more important role in microglia than in other types of brain cells.

Next, the researchers genetically engineered mice that lack microglial HDAC3. knockout mouse. They compared the knockout mice to a control group of mice that retained microglial HDAC3. They induced strokes in both groups of mice for 60 minutes. They then examined the mice's brains using MRI after three, 14, and 35 days to see how the brain damage caused by the stroke progressed in the two different groups. They found that the knockout mice had less brain damage than control mice on all three days.

The researchers also found that the knockout mice had better scores on motor, learning, memory, and behavioral tests than control mice. For example, when scientists applied sticky tape to the soles of mice's feet, the knockout mice removed the tape about 50 seconds faster than control mice. The knockout mice had less myelin loss and less degeneration of electrical pathways in the brain. The researchers interpreted these results to suggest that inhibiting microglial HDAC3 in mice prevented brain damage and improved mental performance after stroke.

The researchers also investigated which gene There were active and inactive forms in two sets of mice. They found that all pro-inflammatory genes tested were inactive in knockout mice, but highly active in mice with microglial HDAC3. They also found that the knockout mice had less activity in genes that produce inflammatory cells.

The researchers concluded that deleting microglial HDAC3 can prevent brain inflammation, myelin removal, and brain tissue damage during stroke. However, before HDAC3 deletion becomes a treatment, they recommended that future researchers determine whether there are any serious side effects. The reduction in inflammation in mice means the same technology could one day be used to reduce the inflammatory effects of stroke in humans.

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