Abstract:
This study investigated the effects of 18bglycyrrhetinic
acid (GA) on neuronal damage in brain tissue
caused by global cerebral ischemia/reperfusion (I/R) in
C57BL/J6 mice. All subjects (n = 40) were equally divided
into four groups: (1) sham-operated (SH), (2) I/R, (3)
GA, and (4) GA?I/R. The SH group was used as a control.
In the I/R group, the bilateral carotid arteries were clipped
for 15 min, and the mice were treated with the vehicle for
10 days. In the GA group, mice were given GA (100 mg/
kg) for 10 days following a median incision without carotid
occlusion. In the GA?I/R group, the I/R model was
applied to the mice exactly as in the I/R group, and they
were then treated with the same dose of GA for 10 days.
Cerebral I/R significantly induced oxidative stress via an
increase in lipid peroxidaitons and a decrease in elements
of the antioxidant defense systems. However, GA treatment
was protective against the oxidative effects of I/R by
inducing significant increases in antioxidant defense systems
and a significant decrease of lipid peroxidations.
Additionally, cerebral I/R increased the incidence of
histopathological damage and apoptosis in brain tissue, but
these neurodegenerative effects were eliminated by GA
treatment. Therefore, the current study demonstrated that
GA treatment effectively prevents oxidative and histological
damage in the brain caused by global I/R. In this
context, GA may be useful for the attenuation of the negative
effects of global cerebral I/R and, in the future, it may
be a viable and safe alternative treatment for ischemic
stroke in humans.
