Kolaviron
was protective against sodium azide (NaN
3
)induced
oxidative stress in the prefrontal cortex
- Publication date
- Publisher
Abstract
Kolaviron is a phytochemical isolated from
Garcina kola (G. kola);
a common oral masticatory agent in
Nigeria (West Africa). It is
a
bioflavonoid used - as an antivi-
ral, anti-inflammatory and antioxidant - in relieving the symp-
toms of several diseases and infections. In this study we have
evaluated the neuroprotective and regenerative effect of
kolaviron in neurons of the prefrontal cortex (Pfc) before or
after exposure to sodium azide (NaN
3
) induced oxidative
stress. Separate groups of animals were treated as follows;
kolaviron (200 mg/Kg) for 21 days; kolaviron (200 mg/Kg
for21days)followedbyNaN
3
treatment (20 mg/Kg for
5days);NaN
3
treatment (20 mg/Kg for 5 days) followed by
kolaviron (200 mg/Kg for 21 days); 1 ml of corn-oil (21 days-
vehicle); NaN
3
treatment (20 mg/Kg for 5 days). Exploratory
activity associated with Pfc function was assessed in the open
field test (OFT) following which the microscopic anatomy of
the prefrontal cortex was examined in histology
(Haematoxylin and Eosin) and antigen retrieval Immunohis-
tochemistry to show astroglia activation (GFAP), neuronal
metabolism (NSE), cytoskeleton (NF) and cell cycle dysreg-
ulation (p53). Subsequently, we quantified the level of
Glucose-6-phosphate dehydrogenase (G6PDH) and lactate
dehydrogenase (LDH) in the brain tissue homogenate as a
measure of stress-related glucose metabolism. Kolaviron
(Kv) and Kolaviron/NaN
3
treatment caused no prominent
change in astroglia density and size while NaN
3
and NaN
3
/
Kv induced astroglia activation and scar formation
(astrogliosis) in the Pfc when compared with the control. Sim-
ilarly, Kolaviron and Kv/NaN
3
did not alter NSE expression
(glucose metabolism) while NaN
3
and NaN
3
/Kv treatment
increased cortical NSE expression; thus indicating stress
related metabolism. Further studies on enzymes of glu-
cose metabolism (G6PDH and LDH) showed that NaN
3
increased LDH while kolaviron reduced LDH in the
brain tissue homogenate
(P<0.001).
In addition
kolaviron treatment before
(P<0.001)
or after
(
P
<0.05) NaN
3
treatment also reduced LDH expression;
thus supporting its role in suppression of oxidative
stress. Interestingly, NF deposition increased in the Pfc
after kolaviron treatment while Kv/NaN
3
showed no sig-
nificant change in NF when compared with the control.
In furtherance, NaN
3
and NaN
3
/Kv caused a decrease in
NF deposition (degeneration). Ultimately, the protective
effect of KV administered prior to NaN
3
treatment was
confirmed through p53 expression; which was similar to
the control. However, NaN
3
and NaN
3
/Kv caused an
increase in p53 expression in the Pfc neurons (cell cycle
dysregulation). We conclude that kolaviron is not neu-
rotoxic when used at 200 mg/Kg BW. Furthermore,
200 mg/Kg of kolaviron administered prior to NaN
3
treatment (Kv/NaN
3
) was neuroprotective when com-
pared with Kolaviron administered after NaN
3
treatment
(NaN
3
/Kv). Some of the observed effects of kolaviron
administered before NaN
3
treatment includes reduction
of astroglia activation, absence of astroglia scars, anti-
oxidation (reduced NSE and LDH), prevention of neu-
rofilament loss and cell cycle regulatio