The scientists say their work lends support to other evidence that ginkgo biloba triggers a cascade of events that neutralises free radicals known to cause cell death. "It is still a large leap from rodent brains to human brains but these results strongly suggest that further research into the protective effects of ginkgo is warranted," says lead researcher Sylvain Doré.
In the study, researchers gave ginkgo biloba EGb 761 - a lab-quality form of the extract - to normal mice and HO-1 knockout mice, mice lacking the gene that produces the enzyme heme oxygenase-1(HO-1). HO-1 breaks down heme, a common iron molecule found in blood, into carbon monoxide, iron and biliverdin. HO-1 has been shown to act as an antioxidant and have a protective effect against inflammation in animal models.
The researchers gave 100 milligrams per kilogram of EGb 761 extract orally once daily for seven days before inducing stroke in the mice. After stroke induction, the mice were tested for brain function and brain damage. One such test, for example, involves running patterns, another tests reaction to an external stimulus. Similar tests were conducted on mice that did not receive the ginkgo extract.
Neurobehavioural function was evaluated before the study and at one, two and 22 hours after stroke using a four-point scale: (1) no deficit, (2) forelimb weakness, (3) inability to bear weight on the affected side, (4) no spontaneous motor activity.
Results showed that normal mice that were pretreated had 50.9 percent less neurological dysfunction and 48.2 percent smaller areas of brain damage than untreated mice. These positive effects did not exist in the HO-1 knockout mice. "Our results suggest that some element or elements in ginkgo actually protect brain cells during stroke," says Doré.
The only current treatment for ischemic stroke is to clear the clot with tissue plasminogen activator (tPA) or other means. This, however, offers no real protection against the cell damage that occurs when blood flow is restored, the researchers say.
MEDICA.de; Source: Johns Hopkins Medicine