Kolaviron was protective against sodium azide (NaN 3 )induced oxidative stress in the prefrontal cortex

Olajide, Olayemi J. and Enaibe, Bernard U. and Bankole,, Oluwamolakun O. and Akinola, Oluwole B. and Laoye, Babafemi J. and Ogundele, Olalekan M. Kolaviron was protective against sodium azide (NaN 3 )induced oxidative stress in the prefrontal cortex. SPRINGER, 30 (1). ISSN 0885-7490

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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 regulation

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