BackgroundMethotrexate (MTX) is a commonly used antineoplastic and anti-rheumatoid agent whose efficacy is limited by marked organ toxicities associated with oxidative stress. The study investigated beneficial effect of virgin coconut oil (VCO) supplementation on MTX-induced oxidative stress and inflammation in rats.MethodsRats were divided into 4 groups (n = 6): Control, MTX (20 mg/kg bw), VCO (5%) + MTX and VCO (15%) + MTX. The pre-treatment with VCO for 14 days was followed by single intraperitoneal injection of MTX and the rats were sacrificed after 3 days. Serum activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), and levels of reduced glutathione (GSH) and malondialdehyde (MDA) were determined. Interleukin-6 (IL-6), C-reactive protein (CRP) and nitric oxide (NO) levels were also evaluated.ResultsMTX induced a distinct diminution in serum activities of oxidative stress markers (SOD, CAT, GPx and GSH), while lipid peroxidation considerably increased demonstrated by MDA level. Similarly, levels of IL-6, CRP and NO increased prominently in MTX control rats. The VCO supplementation markedly enhanced resistance to the MTX-induced biochemical alterations in rats.ConclusionVCO can be a useful adjuvant natural product in MTX chemotherapy by reducing oxidative stress and pro-inflammatory responses.

With the global rise in consumption of western diet, obesity is becoming a pandemic. High fat and high calorie diet (though more palatable) have been associated with a range of metabolic disorders. Oxidative stress and insulin resistance have a link to the dietary etiology of diabetes and obesity; on the other hand, neuroinflammation and abnormal brain insulin signaling is said to cause cognitive decline when high fat diet (HFD) is consumed. In this study, mice were fed a home-made HFD with a total energy content of 5340kcal/kg. The overall energy contribution of saturated and unsaturated fat was about 70%. Animals were divided into Group I and II of 5 mice each. Group I (control group) were fed normal chow and water ad libidum. Group II (test group) were fed HFD and water ad libidum. HFD significantly (p<0.05) increased the body weight of the test group (40 ±7.7) as compared to control (30 ± 2.9). Blood glucose levels in the test group was also significantly higher (111.6 ± 5.2) compared to the control (77.6 ± 8.7). Morris water maze escape latency in the test group was not significantly different (68 ± 26.3) compared to the control (72 ± 20.9). Similarly, the time spent in target quadrant in the test group was not significantly different (20.8 ± 10.9) compared to the control (15.8 ± 5.6). In the Y-maze the control group had a significantly higher (29.6 ± 3.5) percentage alternations compared to the test group (21 ± 13.1). It is obvious that the chronic administration of HFD in mice altered the body's metabolic processes as evident in the significant weight gain, hyperglycemia and cognitive deficit. These can be attributed to the oxidative damage, insulin dysregulation and pro-inflammatory potentials of HFD.

Background: Effect of CBD and omega 3 fatty acid on high fat diet (HFD) induced dementia mice was investigated using Morris water maze (MWM), Elevated plus maze (EPM), Y-maze, Beam walk assay (BWA) and Wire hang test (WHT). Method:Mice were divided into 6 groups of five each. Group I, control had only water and feeds ad libidum; group II-HFD + water, group III-HFD + CBD (10mg/kg/day); group IV-HFD + Omega 3 (200mg/kg/day), group V-HFD, CBD + Omega 3 all for 12 weeks. Group VI had HFD for 12 weeks then back to normal diet + omega 3 for 2 weeks. Frontal lobes were harvested and stained with H and E and congo red. Gene expression was done.Result: Acquisition time in group V was significantly lower compared to others. No difference was noticed in the probe trial. Y-maze alternation was significantly higher in V compared to the II. WHT was significantly shorter in II compared to I, III, IV and V.Closed arm entry time was significantly shorter in II compared to I, III, IV and V. Neuronal count was significantly higher in IV and VI compared to II. No difference in BWA. Gut E.coli was significantly higher in II and VI compared to I, III, IV and V. HFD significantly induced amyloid plaques, neuronal ischemia and significant fold decrease in gene expressions of MAPK-1, IGF-1, ACHe, APOe, Catalase and BDNF. However, CBD and Omega 3 significantly increased their expression. Omega 3 with stoppage of the HFD significantly upregulated the levels of MAPK, BDNF and APOe compared to the others. Conclusion:HFD cause mixed dementia (Alzheimer's and Vascular dementia) and anxiety disorder with suppression of vital brain neurotransmitters and enzymes. CBD and Omega 3 significantly ameliorated these by astrocytosis and upregulating vital genes.In conclusion, chronic HFD administration impairs cognition by multiple molecular mechanisms involving gene suppression which were ameliorated by administration of CBD and Omega 3. Moreso, when HFD was stopped and Omega 3 co-administered with normal diet; pointing to a more reliable way of preventing and treating dementia through reduction in HFD and CBD, Omega 3 supplementation.

Constipation is one of the most common gastrointestinal disorders that affects people of all ages and is mostly treated using orthodox drugs that often have side effects; therefore, this research aims to investigate the effects of a natural product; virgin coconut oil (VCO) in the treatment of loperamide induced constipation in rats. Twenty-five male Wistar rats weighing 80-100 g were divided into 5 groups as follows: Group 1 was control group that received 5 mL/kg/day normal saline (NS) only. All the other groups were treated with 4 mg/Kg loperamide to induce constipation. After 1 hour of loperamide treatment, Group 2 were treated with 5 mL/Kg NS, Group 3, 0.6 mL/day VCO (MVCO); Group 4, 0.9 mL/day VCO (HVCO) and Group 5 rats, 2 mg/Kg bisacodyl. The period of treatment was 3 days, and they were administered orally. Daily food consumption, number, weight and water content of feces, and intestinal transit time of charcoal meal were determined. Result showed that food consumption was significantly (P < 0.05) lower in loperamide alone group than other groups of animals. By days 1 and 3, the number of fecal pellets, weight of wet feces, weight of dry feces, and water content of feces in MVCO treated and control rats were significantly (P <0.05) higher than loperamide +NS. The intestinal transit time in MVCO treated rats (54.47 ± 3.22%) was however not significantly different from loperamide + NS (56.51 ± 2.51%). In conclusion, VCO ameliorated loperamide induced constipation by increasing the frequency of defecation, weight and water content of feces.

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Arsenic (As) is a classic neurotoxicant; its pathogenesis is associated with oxidative stress and oxidative stress-mediated cholinergic deficits. This study explored antioxidant activity of virgin coconut oil (VCO) against sodium arsenite-induced oxidative stress-mediated cerebral neurotoxicity in rats. Eighteen rats were divided into 3 groups- Normal control, As control and VCO + As. The VCO (5 mL/kg) was given once daily by oral gavage from day 1 to day 21, while As (10 mg/kg) was given once daily by oral gavage from day 15 to day 21. Cerebral superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), malondialdehyde (MDA), adenosine deaminase (ADA) and acetylcholinesterase (AchE) activities were analysed. Nitric oxide (NO), lipid profile, phospholipid (PL), and reduced glutathione (GSH) were also evaluated in cerebral homogenate. The cerebrum was sectioned for histological analysis. Administration of As induced significant depressions in antioxidant enzymes, GSH, PL, and HDL-c compared to normal control. Levels of MDA, NO, total cholesterol and activities of ADA, AchE in the cerebrum were markedly increased by As compared to normal rats. Lipid profile indices and PL were prominently altered by As. Histopathological study supported the biochemical findings through extensive cerebral damage. In contrast, oral supplementation of VCO prior to and along with As treatment significantly attenuated the As-induced biochemical alterations and restored near-normal histology. VCO attenuates cerebral neurotoxicity by strengthening endogenous antioxidant defence and cholinergic function via counteracting free-radical-mediated arsenic toxicity.

L-N G -Nitro arginine methyl ester (L-NAME) was used to induce hypertension in this experiment and the intervention plant extract was Adansonia digitata fruit. A total of 30 rats were used for this research and divided into 6 groups of 5 animals each. Group 1 was control (water and feed ad libidum), group 2 (L-NAME), group 3 (ramipril 10 mg/kg), group 4 (A. digitata 200 mg/kg), group 5 (A. digitata 400 mg/kg) and group 6 (A. digitata 400 mg/kg no induction). Extract administration lasted 21 days after which animals were anesthetized and blood samples taken for analyses. Prior to this, recordings of blood pressure and weights were recorded. The fruits extract of the baobab plant was found to significantly reduce (P<0.05) the blood pressure in the hypertensive animals compared to the control and test drug. The Na and Cl concentrations in blood were significantly reduced compared to the control and L-NAME group at dose of 400 mg/kg. It was also found to prevent hyperkalemia and normalized creatinine as well as serum protein levels. The extract also significantly reduced the body weight of the animals at same dose. In conclusion, the extract reduced blood pressure in this experiment by reduction of Na (salt) concentration. It is a promising plant that will help sufferers from hypertension. Further studies are needed to study about molecular mechanisms involved in its activities.

This article reveals trend of HIV/AIDS in Benue State, north central, Nigeria. The method adopted was a descriptive analysis of the HIV epidemiology in Nigeria using Benue State as a case study. This review article was through the report of periodic epidemiological surveys of Antenatal Clinic (ANC) sentinel surveys, National HIV and AIDS and Reproductive Health Surveys (NARHS), Nigeria Demographic Health Surveys (NDHS), Integrated Biological and Behavioural Surveillance Surveys (IBBSS), National Agency for the Control of AIDS (NACA), United Nations Agency for AIDS (UNAIDS) and Benue State Agency for the Control of AIDS (BenSACA). This study reveals that, out of the current 1.9 million people representing 1.4% (15-49 years) living with HIV in Nigeria, Benue State accounts for 188,482 representing 4.9%. Thus, Benue State is now second as against the previous reports which have consistently placed Benue State as the state with highest prevalence of HIV/AIDS in Nigeria since the beginning of the pandemic in the country. The new prevalence estimates by states, however, still categorize Benue state and six other states with high prevalence of 2.0% and above. The national prevalence among females is significantly higher at an estimated 1.9% than the male prevalence estimated at 0.9%. In conclusion, the effort of peer educator trainers, awareness of HIV/AIDS on radio and television programs and efforts of other stake holders who are working towards ending the AIDS epidemic have been the secret behind the compliance of Benue people towards spreading news of AIDS not the virus. However, much still need to be done to consolidate on this success.