Strokes inflict 80% less brain damage in mice lacking a DNA repair enzyme, according to a report in the issue of this month Nature Medicine . In normal mice, the enzyme zealous deprives brain cells of energy - trying to repair damaged DNA - for hours after a stroke. The discovery suggests that an enzyme inhibitor may prevent damage in humans after existing drugs have restored blood flow
During a stroke, blood flow to part of the brain is cut off. - So that supply oxygen and nutrients such as sugar. Most stroke research has focused on restoring oxygen to the brain, says Valina Dawson, a neuroscientist at Johns Hopkins University. But research has shown that brain cells continue to die after blood flow is restored, since the renewed metabolism generates free radicals that damage DNA and other cell parts. In response, the cells activate an enzyme called poly (ADP-ribose) polymerase (PARP) to repair DNA damage. Dawson said that to try to repair the DNA of the cell, PARP could seriously deplete energy resources and perhaps even kill the cell.
Dawson and his team first have to mice brain cell cultures that have been bred not to produce PARP. Even when the cells were starved of oxygen and sugar, or exposed to chemicals which release neurotoxins such as nitric oxide, they are not damaged - that up to 65% of the cells from normal mice death when subjected to similar treatment. When the researchers then induced stroke in mice with or without the PARP gene, they found that tissue damage resulting from the mice without the enzyme was 80% less than in normal mice. "The protection was phenomenal and beyond our best expectations," said Dawson. Most tests of drug animal stood between 10% to 30% less damage, and sometimes up to 50%, she added.
The protective effect of PARP inhibition is "striking" and made "a strong case" to examine the role of PARP in the human race, said Thomas Jacobs, a neuroscientist at the National Institute of neurological disorders and Stroke in Bethesda, Maryland.
0 Komentar