Leaf extract of Anacardium occidentale ameliorates biomarkers of neuroinflammation, memory loss, and neurobehavioral deficit in N(ω)-nitro-L-arginine methyl ester (L-NAME) treated rats.

PURPOSE: Anacardium occidentale commonly known as Cashew is a plant that is widely used in African traditional medicine. It is endowed with phytochemical constituents that are responsible for its medicinal properties. METHODS: Twenty-five male Wistar rats were grouped as follows: Control (Group A), Group B (L-NAME 40 mg/kg), Group C (100 mg/kg Anacardium occidentale extract plus 40 mg/kg L-NAME), Group D (200 mg/kg extract plus 40 mg/kg L-NAME) and Group E (10 mg/kg of Lisinopril plus 40 mg/kg L-NAME). The animals were treated with oral administration of either the extracts or Lisnopril daily for 4 weeks. Neuro-behavioural tests such as the Morris Water Maze and Hanging Wire Grip tests were carried out to evaluate memory/spatial learning and muscular strength, respectively. Makers of oxidative stress, antioxidant enzymes and immunohistochemical staining of Glial Fibrillary Acidic Protein and Ionised Calcium Binding Adaptor molecule 1 were assessed. RESULTS: L-NAME administration caused significant increases in biomarkers of oxidative stress, decreased antioxidant status, acetylcholinesterase activity, altered neuro-behavioural changes, astrocytosis, and microgliosis. However, Anacardium occidentale reversed exaggerated oxidative stress biomarkers and improved neuro-behavioural changes. CONCLUSIONS: Combining all, Anacardium occidentale enhanced brain antioxidant defence status, improved memory and muscular strength, thus, suggesting the neuroprotective properties of Anacardium occidentale.

Neurocognitive domains and neuropathological changes in experimental infection with Trypanosoma brucei brucei in Wistar rats.

Trypanosoma brucei brucei causes animal trypanosomiasis in several vertebrates and human African trypanosomiasis. Previous studies have only explored the incidence, clinical symptoms, haematology and biochemical changes associated with the disease. The behavioral manipulation hypothesis posits that parasites alter the behavior of host to increase the reproductive abilities of such parasites. Hence, the present study was carried out to investigate changes in behavior and cognition following experimental infection of T. brucei brucei in rat model. This study involved two groups of animals (uninfected control and T. brucei infected) with 8 rats per group. After confirmation of parasitaemia in the infected rats both groups were assessed to investigate if infection led to behavioral alterations and neuropathological changes using the open field, social interaction and forelimb suspension tests. Immunohistochemistry was performed on brain tissues using glial fibrillary acidic protein and anticalbindin-D28k, antibodies. We demonstrated that T. brucei infection triggered a significant decrease in exploratory activity, anxiety-like behavior, altered recognition of social novelty and reduced hanging latency in the hanging wire test. Immunohistochemistry revealed significant astrocytosis, loss of dendritic spines and reduction of Purkinje cell layer of the cerebellum. These results demonstrate that T. brucei infection induce signs of anxiety, impaired motor co-ordination with degeneration and loss of Purkinje cells.

Luteolin supplementation ameliorates cobalt-induced oxidative stress and inflammation by suppressing NF-кB/Kim-1 signaling in the heart and kidney of rats.

Cobalt-induced cardiomyopathy and renal toxicity have been reported in workers in processing plants, hard metal industries, diamond polishing and manufacture of ceramics. This study was designed to investigate the influence of Luteolin supplementation on cobalt-induced cardiac and renal toxicity in rats. Exposure of rats to cobalt chloride (CoCl2) alone caused significant (p < 0.05) increases in cardiac and renal H2O2, malondialdehyde (MDA) and nitric oxide (NO), along with increased serum myeloperoxidase (MPO) activity. In addition, there were significant (p < 0.05) reductions in cardiac and renal glutathione peroxidase (GPx), glutathione S-transferase (GST) and reduced glutathione (GSH). CoCl2 induced higher immuno-staining of nuclear factor kappa beta (NF-κB) in the heart and kidneys, and the kidney injury molecule (Kim-1) in the kidneys. Treatment with Luteolin or Gallic acid produced significant reversal of the oxidative stress parameters with reductions in NF-κB and Kim-1 expressions, leading to suppression of histopathological lesions observed in the tissues.

Βeta-sitosterol enhances motor coordination, attenuates memory loss and demyelination in a vanadium-induced model of experimental neurotoxicity.

Environmental discharge of vanadium causes cognitive and behavioral impairments in humans and animals via production of reactive oxygen species leading to lipid peroxidation and alteration in antioxidant defence system. The current study was carried out to investigate the cognitive-enhancing ability of ß-sitosterol in vanadium-induced neurotoxicity. Forty eight mice were randomly assigned into 4 groups (A-D) with the following treatments: group A; distilled water, B; α-tocopherol + sodium metavanadate (NaO3V), C; ß-sitosterol + NaO3V and D; only NaO3V. NaO3V was administered intraperitoneally while other treatments were administered through gavage for 7 consecutive days. Neurobehavioral parameters measuring cognition, locomotion, anxiety and grip strength were evaluated at day 8. Following sacrifice, brain levels of catalase, superoxide dismutase, glutathione, malonaldehyde (MDA) and hydrogen peroxide (H2O2) were measured. Immunohistochemical expression of Myelin Basic Protein (MBP) in the brain was also investigated. The results showed that deficits in spatial learning, locomotor efficiency, and motor coordination, induced by acute vanadium neurotoxicity were mitigated by beta-sitosterol. Significantly (α ≤ 0.05) decreased in vivo antioxidant enzyme activities, increased brain levels of MDA and H2O2, structural damage to myelin sheaths and decreased expression of MBP were also observed in the NaO3V group (D), however, co-administration of ß-sitosterol reduced these pathologic features. It is concluded that ß-sitosterol alleviates vanadium-induced neurotoxicity by enhancing cognition and improving motor co-ordination via its antioxidant and myelo-protective activities.

Sodium metavanadate induced cognitive decline, behavioral impairments, oxidative stress and down regulation of myelin basic protein in mice hippocampus: Ameliorative roles of ß-spinasterol, and stigmasterol.

INTRODUCTION: Exposures to toxic levels of vanadium and soluble vanadium compounds cause behavioral impairments and neurodegeneration via free radical production. Consequently, natural antioxidant sources have been explored for effective and cheap remedy following toxicity. Grewia carpinifolia has been shown to improve behavioral impairments in vanadium-induced neurotoxicity, however, the active compounds implicated remains unknown. Therefore, this study was conducted to investigate ameliorative effects of bioactive compounds from G. carpinifolia on memory and behavioral impairments in vanadium-induced neurotoxicity. METHODS: Sixty BALB/c mice were equally divided into five groups (A-E). A (control); administered distilled water, B (standard); administered α-tocopherol (500 mg/kg) every 72 hr orally with daily dose of sodium metavanadate (3 mg/kg) intraperitoneally, test groups C, and D; received single oral dose of 100 µg ß-spinasterol or stigmasterol (bioactive compounds from G. carpinifolia), respectively, along with sodium metavanadate and the model group E, received sodium metavanadate only for seven consecutive days. Memory, locomotion and muscular strength were accessed using Morris water maze, Open field and hanging wire tests. In vivo antioxidant and neuroprotective activities were evaluated by measuring catalase, superoxide dismutase, MDA, H2 O2 , and myelin basic protein (MBP) expression in the hippocampus. RESULTS: In Morris water maze, stigmasterol significantly (p ≤ 0.05) decreased escape latency and increased swimming time in target quadrant (28.01 ± 0.02; 98.24 ± 17.38 s), respectively, better than α-tocopherol (52.43 ± 13.25; 80.32 ± 15.21) and ß-spinasterol (42.09 ± 14.27; 70.91 ± 19.24) in sodium metavanadate-induced memory loss (112.31 ± 9.35; 42.35 ± 11.05). ß-Spinasterol and stigmasterol significantly increased exploration and latency in open field and hanging wire tests respectively. Stigmasterol also increased activities of antioxidant enzymes, decreased oxidative stress markers and lipid peroxidation in mice hippocampal homogenates, and increased MBP expression. CONCLUSIONS: The findings of this study indicate a potential for stigmasterol, a bioactive compound from G. carpinifolia in improving cognitive decline, motor coordination, and ameliorating oxidative stress in vanadium-induced neurotoxicity.

Hematology and erythrocyte osmotic fragility of the Franquet's fruit bat (Epomops franqueti).

Background Hematological parameters are vital diagnostic tools for understanding health dynamics of humans and animals. Franquet's fruit bat (Epomops franqueti) is host to several parasites such as protozoa, bacteria, viruses and mites. Yet, studies exploring the values of its blood components with interest for research or food purposes are scarce. Thus, this study was carried out to investigate the hematological values of the adult E. franqueti. Methods Seventeen (nine female and eight male) apparently healthy adult E. franqueti were captured from their roosting colony. Blood samples were collected for determination of erythrocyte indices [red blood cell count (RBC), packed cell volume (PCV), hemoglobin (Hb) concentration, mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH) and mean corpuscular hemoglobin concentration (MCHC)] and leukocyte indices [total white blood cell counts (WBC), lymphocytes, eosinophil, monocytes, neutrophil count and erythrocytes osmotic fragility]. Results There were no significant (p≥0.05) sex-related differences in RBC, PCV, Hb concentration, MCV, MCH, MCHC and total and differential WBC of E. franqueti. Erythrocyte osmotic fragility was significantly higher in female than in male E. franqueti at 0.1% NaCl. Conclusions These considerations are critical in establishing reference ranges of blood parameters for E. franqueti and may provide insight to why they serve as reservoir hosts for several microorganisms.