The authors of the new work studied how anti-cancer drugs and other drugs could be used alternatively.
And the work of this same region of DNA is disrupted during the development of chronic pain. Therefore, the researchers concluded that normalizing KCC2 activity would reduce chronic pain.
They used a culture of mouse neurons tostudy how about a thousand different anti-cancer drugs work. Their genome was modified so that the cells began to glow when the KCC2 gene was activated.
We have screened a large number of anticancer drugsdrugs that affect the process of cell growth, in the hope of finding a substance that would affect the KCC2 gene, whose activity in neurons decreases with the development of chronic pain. Our searches indicated that the drug kenpaullone has such properties.
Research text
The authors chose the drug Kenpaullon: it was able to block chronic pain that appeared due to the penetration of cancer cells into the bones of mice, as well as due to damage to the spinal cord.
It is noted that kenpaullone did not act like opioids, which simply block pain.
The drug did not directly affect the KCC2 gene, butsuppressed the work of the enzyme GSK3-beta, whose molecules prevent the normal activation of this DNA region. Thanks to this, scientists have created an experimental gene therapy that forever relieves rodents from chronic pain.
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