Glia activation and neuroinflamation are major factors implicated in the aetiology of most neurodegenerative diseases (NDDs). Several agents and toxins have been known to be capable of inducing glia activation an inflammatory response; most of which are active substances that can cause oxidative stress by inducing production of reactive oxygen species (ROS). Neurogenesis on the other hand involves metabolic and structural interaction between neurogenic and glia cells of the periventricular zone (PVZ); a region around the third ventricle. This study investigates glia activation (GFAP), cell proliferation (Ki-67) and neuronal metabolism (NSE) during neurogenesis and oxidative stress by comparing protein expression in the PVZ against that of the parietal cortex. Adult Wistar Rats were treated with normal saline and 20 mg/Kg KCN for 7 days. The tissue sections were processed for immunohistochemistry to demonstrate glia cells (anti Rat-GFAP), cell proliferation (anti Rat-Ki-67) and neuronal metabolism (anti Rat-NSE) using the antigen retrieval method. The sections from Rats treated with cyanide showed evidence of neurodegeneration both in the PVZ and cortex. The distribution of glia cells (GFAP), Neuron specific Enolase (NSE) and Ki-67 increased with cyanide treatment, although the increases were more pronounced in the neurogenic cell area (PVZ) when compared to the cortex. This suggests the close link between neuronal metabolism and glia activation both in neurogenesis and oxidative stress.

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Obesity is a metabolic dysfunction triggered by refined carbohydrate and high-fat-rich foods, as well as sedentary lifestyle. It can also be as a result of increased calorie intake and reduced calorie expenditure mediated through environmental, genetic, epigenetic and neuropsychological factors (Castro et al., 2017;Leisegang et al., 2019). It is usually characterised by increased visceral adiposity (Agarwal et al., 2018). Obesity has become an epidemic in recent decades, with millions of people worldwide suffering from the disease. Recent data from the World Health Organization showed that over 1.9 billion adults are either overweight or obese, with 650 million adults typically obese (World Health Organization, 2018).

In this study, gas chromatography-mass spectrometry (GC/MS) was used to analyse the isolated caffeine from kolanut and deternine the acute and chronic toxicity of the extract and the isolated caffeine. In chronic toxicity test, rats were divided into five groups (10 rats per group). Each rat was administered with normal saline (control group), crude kolanut extract (11.9 mg/kg), isolated caffeine (7.5 mg/kg), synthetic caffeine (6 mg/kg) or (6 mg/kg) decaffeinated kolanut extract orally for 90 days. Biochemical assessment and body weight of the rats were determined. In acute test, the limit test dose of 2000 mg/kg was administered to the rat and observed for 48 h post treatment. This dose caused behavioural changes but did not cause mortality in the rats tested. The results of the chronic administration showed that caffeine significantly (P < 0.05) decreased body weight. Liver enzymes were significantly (P < 0.05) increase, total plasma protein levels, creatinine, bilirubin, very low density lipoprotein (VLDL), low density lipoprotein (LDL) and total serum cholesterol levels were also significantly (P < 0.05) higher. However, urea was significantly (P < 0.05) lower in the caffeine treated groups. The results of the GC-MS analysis showed that the isolated caffeine from kolanut extract contains 82.69% pure caffeine with 96% in quality. Our results showed that the kolanut extract is rich in high quality caffeine and chronic consumption of it is associated with significant toxic effects as shown by elevated biochemical parameters, and reduction in body weight.

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