Drug that prevents premature birth in mice could be used on humans: Aussie study
Xinhua, November 8, 2016 Adjust font size:
Australian researchers are hopeful that an experiment which entirely prevented premature births in mice could be applied to humans.
The team from the Robinson Institute at the University of Adelaide were able to entirely suppress the inflammatory mechanisms that can lead to premature births by using plus-naloxone, a drug known to block pro-inflammatory pathways.
Sarah Robertson, director of the Robinson Institute and lead author of the study, said that the team recorded a significant reduction in infant mice fatalities - and a reversal in the low birth-weight associated with premature birth.
"The babies born to mothers treated with plus-naloxone developed normally and were mostly indistinguishable from those born to the control group," Robertson told the Australian Broadcasting Corporation (ABC) on Tuesday.
"Not only did we prevent them being born too soon, we prevented stillbirth and the foetal growth restriction that would otherwise have occurred.
"(It's) unusual to find a single molecule in biology that has such a potent effect."
Premature birth is caused in humans due to an "inflammatory cascade" caused by bacterial infection, physical injury, and placental damage which can activate an immune response in pregnant women who will then be unable to carry their baby beyond 37 weeks.
Robertson said plus-naloxone prevented the inflammatory response from occurring in mice and it could do the same in humans, but it would be years before it was tested on humans.
"The exciting thing is that these drugs have already been tested in people with infections," Robertson said.
"Prospects for bringing them to human use are close but it will be several years I guess before we can have the confidence to test them in women who are pregnant."
The Robinson Institute said being born premature was the biggest cause of death for children under the age of five, accounting for 1.1 million deaths, worldwide every year. Endit