Sci Adv: University of Pittsburgh: New small protein drug to reduce stroke sequelae and protect the brain

Strokestroke(Stroke) commonly known as stroke, including ischemic stroke (brain infarction) and hemorrhagic stroke (brain haemorrhage, ventricular haemorrhage, cobweb subcavity bleeding)It has the characteristics of morbidity, disability, recurrence and mortalityStroke is the number one cause of death among Chinese residentsIschemic stroke accounts for 75%-90% of all strokes, while hemorrhagic stroke accounts for only 10-25%And the after-effects of stroke patients are difficult to treatneuroscientists at the University of Pittsburgh's Brain Institute have discovered a new drug that protects the brain during and after a strokestudy published July 1 in the journal Science Advance sshown that damaged neurons can still survive if they do not follow the biochemical pathways that cause cell death"In clinical practice, there is no drug that can prevent cell death after a stroke," said Anthony Schulien, a medical student atthePitt School of Medicine's training program and lead author of the studyThese trials provide exciting early evidence for drug targeting, which we hope will one day be applied to patientsProfessor of Neurobiology and senior author DrElias Aizenman, professor of neurobiology at Pitt School of Medicine, explains that strokes occur becauseblood clots in the brain block blood vessels , preventing blood and oxygen from reaching neurons and killing them Neurons nearby, known as the stroke semi-dark zone, may also have dysfunction and die after hours or days, even if their blood oxygen supply is only slightly or briefly reduced "We're also looking for ways to prevent other neuronal deaths, and if we can do that, recovery may improve, and we may be better able to help stroke patients whose blood clots are unable to enter blood vessels or get to the hospital in time for early intervention," said Ezeman With the right drugs, we may also be able to slow the progression of known strokes before patients arrive at the hospital in a previously published study, Ezeman's team showed that the interaction between the potassium ion channel Kv2.1 and the synth protein in the cell membrane causes potassium ions to leak out of neurons, causing cell death They found that using an experimental compound called TAT-C1aB could prevent cell death by interfering with the interaction of synths and Kv2.1 In this new study, researchers identified two types of Kv2.1 channels in the membranes of neuronal cells One channel is usually associated with cell excitability, while the other allows additional, new Kv2.1 channels to enter the cell membrane, promoting the release of potassium and eventually causing neuronal cell death with this knowledge, scientists have created a new small protein called TAT-DP-2, which can disrupt these new channels into the cell membrane, leaving potassium ions in cells and preventing the biochemical pathways in which cells die TAT-DP-2 inhibits apoptosis Kv2.1 electrical shock in vitro and has a neuroprotective effect
the abdominal cavity injection TAT-DP-2 can reduce the volume of cerebral infarction
after stroke injection TAT-DP-2 mice with a smaller stroke damage area, long-term nerve function is better than in the uninjected mice Two completely different approaches using Kv2.1 can improve stroke outcomes, suggesting that the prospect of a neuroprotective drug for the channel is promising