Spider venom will help treat a stroke
Spider Venom component reduced brain damage after stroke
Oleg Lischuk, N+1
Australian scientists have discovered that a component of the venom of one of the local spiders can prevent the death of nerve cells in ischemic stroke. The results of the work are published in the journal Proceedings of the National Academy of Sciences (Chassagnon et al., Potent neuroprotection after stroke provided by a double-knot spider-venom peptide that inhibits acid-sensing ion channel 1a).
Psalmopoeus cambridgei
Ischemic stroke, or cerebral infarction (thrombosis of one or more arteries of the brain with the death of a section of its tissue) is the second most common cause of death and disability of the world's population after myocardial infarction. Brain damage in stroke has two distinct zones: central necrosis (rapid cell death in the immediate vicinity of a blood clot) and periinfarction, in which cell death occurs within hours or even days, so theoretically it can be prevented by timely treatment. Treatment in the acute period is carried out either by pharmacological dissolution of the thrombus (fibrinolysis), or by intravascular removal, but these methods are not always available and are suitable only for a small number of patients.
The main mechanism of damage to neurons in the periinfarction zone is their transition to anaerobic glycolysis in conditions of oxygen deficiency. This leads to an increase in the acidity (that is, a decrease in pH) of the intercellular medium and activation of acid-sensitive ion channels 1a (ASIC1a) – the main mediators of ischemic damage to neurons with subsequent apoptosis (programmed death). In animal experiments, switching off the gene encoding ASIC1a reduced the size of post-stroke necrosis by about 60 percent. Pharmacological blockade of these channels was significantly less effective. The most effective of the detected agents was the tarantula venom Psalmopoeus cambridgei, which contains 0.4 percent PcTx1 – selective inhibitor of ASIC1a. However, this poison acts only in the first two to four hours after a stroke, while the growth of the necrosis zone lasts much longer.
In search of a more effective ASIC1a inhibitor, the staff of the Universities of Queensland and Monash conducted an analysis of the transcriptome of the Australian spider Hadronyche infensa. He revealed the presence of four non-toxic peptides having structural similarity to PcTx1. The peptide Hi1a showed the greatest similarity.
Hi1a structure (here and below are the figures from the PNAS article)
In experiments on cell cultures expressing rat and human ASIC channels, this substance strongly inhibited ASIC1a (but not other subtypes), and it acted several times longer than PcTx1. The introduction of Hi1a into the ventricle of the rat brain after an artificially induced stroke significantly reduced the area of necrosis, not only in the periinfarction (cerebral cortex), but also in the central (striatum) zone. The volume of observed neurological disorders decreased accordingly. Moreover, the drug was effective even when administered eight hours after arterial thrombosis, as can be seen in the graphs.
Reduction of brain damage and neurological disorders with the introduction of Hi1a
"We believe that for the first time we have found a way to minimize brain damage after a stroke," said Glenn King, the head of the work, and added that his laboratory will make every effort to bring Hi1a research to the clinical trial stage as quickly as possible.
Other research teams have also achieved some success in the treatment of post-stroke disorders. Thus, the partial restoration of brain tissue was facilitated by the appointment of anakinra receptor antagonist to interleukin-1, stimulation of nerve fiber myelination and the introduction of stem cells.
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22.03.2017