Gestational and neurodevelopmental effects of black mustard seeds’ (Brassica nigra) extract in wistar rats

This study investigated the effect of the crude aqueous extract of Brassica nigra (Black Mustard Seeds) in gestation and on the prefrontal cortex of newborn Wistar rats at different doses following prenatal administration. Eighteen (18) adult female rats weighing an average of 180±10g were used. The female rats were split into 3 groups of six animals; Group A received distilled water throughout gestation, Group B received 200 mg/kg body weight of extract throughout gestation, and Group C received 100 mg/kg body weight of extract throughout gestation). Rat pups from the experimental groups were sacrificed on postnatal days 1, 7, 14, 21, 28, and 35 and subsequently prepared through routine histological and histochemical procedures. Brassica nigra was abortifacient at 200 mg/kg body weight and reduced litter size at 100 mg/kg body weight. No observed physical deformities in pups of treated groups. Comparative prefrontal microarchitecture revealed little to no alteration in the treated group. This study concludes that Brassica nigra (black mustard) is not totally innocuous and as such, should be moderately consumed or totally avoided in pregnancy.Keywords: Brassica nigra; Mustard seeds; Gestation; Neurodevelopment

Gestational and neurodevelopmental effects of black mustard seeds' (Brassica nigra) extract in wistar rats

This study investigated the effect of the crude aqueous extract of Brassica nigra (Black Mustard Seeds) in gestation and on the prefrontal cortex of newborn Wistar rats at different doses following prenatal administration. Eighteen (18) adult female rats weighing an average of 180±10g were used. The female rats were split into 3 groups of six animals; Group A received distilled water throughout gestation, Group B received 200 mg/kg body weight of extract throughout gestation, and Group C received 100 mg/kg body weight of extract throughout gestation). Rat pups from the experimental groups were sacrificed on postnatal days 1, 7, 14, 21, 28, and 35 and subsequently prepared through routine histological and histochemical procedures. Brassica nigra was abortifacient at 200 mg/kg body weight and reduced litter size at 100 mg/kg body weight. No observed physical deformities in pups of treated groups. Comparative prefrontal microarchitecture revealed little to no alteration in the treated group. This study concludes that Brassica nigra (black mustard) is not totally innocuous and as such, should be moderately consumed or totally avoided in pregnancy.Keywords: Brassica nigra; Mustard seeds; Gestation; Neurodevelopment

Moringa Regimen Corrects Nicotine-induced Deficits in Behaviour, Altered Energy Metabolism and Neurotransmitter Processing in Rat Brain

Background: Nicotine is the addictive component of tobacco smoking. It has been reported to have a negative neuromodulatory role in the CNS. Moringa oleifera is a medicinal plant with reported antioxidant, anticonvulsant, anti-inflammatory and neuroprotective properties. Aim and Objectives: This study was purposed to investigate the neuronal adaptation potentials of Moringa Oleifera (MO) on nicotine induced behavioural decline and perturbed bioenergetics. Material and Methods: Twenty-four adult male Wistar rats were used. The treatment regimen was as follows; control group received distilled water, MO group received 200 mg/kg of MO, Nicotine Group received 1.38 mg/kg body weight of nicotine, and Nicotine + MO group received combined treatment of 200 mg/kg body weight of MO after 1.38 mg/kg body weight of nicotine for 28 days. The animals were subjected to Morris water maze for spatial memory, Y maze for working memory and elevated-plus maze tests for anxiety levels after which they were sacrificed for spectrophotometric analysis of global protein expression, neural bioenergetics (lactate dehydrogenase and glucose-6-phosphate dehydrogenase), and Acetylcholinesterase (AChE) levels. Results: Nicotine infusion caused a reduction in the escape latency period, increased the percentage incorrect alternation, and elevated the anxiety levels of rats. These observations were indicative of decreased synaptic activity in the brain. Together with, nicotine induced chromatolytic changes in cells of the frontal cortex and hippocampus. Co-administration with MO prevented nicotine-associated memory decline, perturbed glucose bioenergetics, induced chromatolysis and histomorphological distortion in the frontal cortex and hippocampus. Conclusion: Our data demonstrate that MO administration enhances experience-dependent neuroplasticity and cognitive behaviour function in laboratory animals, modulates energy metabolism and reduced oxidant stress possibly through enhanced production of key antioxidant enzymes against the damaging effects of nicotine. It provided evidence that MO can be further developed as a means to protect the brain from oxidative stress-induced injury

Comparison of Indices of Insulin Resistance and Islet Beta-Cell Dysfunction across Rat Models of Diabetes Mellitus Induced by Modified Diets or Streptozotocin

Background: Induction of insulin resistance in rodents involves the use of Streptozotocin (STZ) or diets high in sucrose, fat or fructose; but the relative degrees of insulin resistance induced by each of these approaches are unclear. Aim and Objectives: We therefore compared the degree to which intraperitoneal STZ with or without high-fat or high-fructose diet would induce insulin resistance, glucose intolerance and islet β-cell dysfunction in Wistar rats. Materials and Methods: Subsets of STZ-injected rats administered streptozotocin at 30 mg/kg body weight for five successive days were fed normal diet (STZ), or diets high in fat or fructose for 30 or 60 days. Normoglycaemic rats on normal rodent chow, High Fat Diet (HFD) or High Fructose Drink (HFrD) constituted the Control (CTR), HFD or HFrD groups, respectively. Rats were anaesthetized and sacrificed at 30 or 60 days of high fat or fructose feeding followed by measurement of fasting plasma glucose and insulin; and calculation of the HOMA-IR and HOMA-%β. Oral Glucose Tolerance Test (OGTT) was done 48 hours prior to killing the animals. Results: Glucose tolerance and islet β-cell function were most severely perturbed in the STZ-injected hyperglycaemic rats fed diets high in fructose or fat, as indicated by the significantly increased (p<0.05) HOMA-IR or decreased HOMA- %β (p<0.05) at 30 or 60 days compared with the CTR, STZ or diet-only groups. Weekly blood glucose was most markedly and significantly (p<0.05) elevated in these same (STZ+diet) groups, with impaired OGTT. Conclusion: The profound impairment of glucose tolerance and β-cell function in the STZ-induced hyperglycaemic rats fed high-fat or high-fructose diet support the continued use of such models in the characterization of the molecular events associated with insulin resistance, and the testing of novel therapeutic interventions