Vitamin D attenuates monosodium glutamate-induced behavioural anomalies, metabolic dysregulation, cholinergic impairment, oxidative stress, and astrogliosis in rats.

BACKGROUND: Monosodium glutamate (MSG) is a commonly used flavor enhancer that has raised concerns due to its potential adverse effects on various organs. This study explored the neuroprotective potential of Vitamin D, a beneficial micronutrient, in mitigating MSG-induced neurotoxicity. MATERIALS AND METHODS: Adult male Wistar rats were categorized into five groups: control (2 ml/kg PBS orally for 30 days), MSG (40 mg/kg orally for 30 days), VIT-D (oral cholecalciferol; 500 IU/kg for 30 days), MSG+VIT-D (MSG for 30 days followed by VIT-D for another 30 days), and VIT-D/MSG (concurrent VIT-D and MSG for 30 days). The rats underwent neurobehavioral, histochemical, and biochemical analyses following the treatments. RESULTS: MSG treatment caused a decline in both long and short-term memory, along with reduced exploratory and anxiogenic behavior, mitigated by vitamin D treatment. MSG exposure also induced impaired behavior, dyslipidemia, oxidative stress, lipid peroxidation, altered cholinergic transmission, and increased chromatolysis and neuroinflammation in the frontal cortex, hippocampus, and cerebellum. CONCLUSIONS: VIT-D demonstrated a mitigating effect on MSG-induced adverse outcomes, highlighting its potential to attenuate neurodegenerative cascades. This investigation contributes to understanding MSG-associated neurotoxicity and suggests vitamin D as a valuable and potential intervention for neuroprotection.

Mucuna pruriens seed repeals the hypothalamic-pituitary-testicular axis disruption following carbamazepine treatment in male Wistar rats.

This study examined the potential effects of Mucuna pruriens (MP) seed powder on the disruptions of the hypothalamic-pituitary-testicular axis caused by the carbamazepine (CBZ) treatment in male Wistar rats. A total of 35 male Wistar rats were randomized into 5 groups (n=7). The animal in group 1 received normal saline (0.2 ml) orally, while groups 2-5 received carbamazepine (CBZ) 25 mg/kg per oral. Groups 1, and 2 were fed with standard rats' chow, while groups 3-5 rats were supplied with a diet containing MP seed powder at 2.25 g, 1.5 g, and 0.75 g respectively. The serum level of male reproductive hormones, estradiol, seminal profiles, and histoarchitecture of the hypothalamus, pituitary, and testis was delineated. Descriptive and inferential statistics were used to analyze the result. There was a marked decrease in the testicular weight, follicle-stimulating hormone, testosterone concentration, and normal sperm cells in the CBZ, and CBZ + MP (2.25 mg/kg) treatment groups.  There was a marked increase in the testicular tissue lipid peroxidation in the CBZ, and CBZ + MP (g) treated rats in addition to various morphological alterations in the hypothalamus, pituitary, and testis. These anomalies were receded in the CBZ + MP (1.5 g), and CBZ + MP (0.75 g) treatment groups. Consumption of MP (1.5 g, and 0.75 g) may alleviate the injurious effects of CBZ treatment on the hypothalamic-pituitary-testicular functions.

Mucuna pruriens seed protects the hippocampal neurons and abrogates seizure indices in chemically-convulsed mice: Evidence of the Nrf2 expression defense pathway.

The anti-convulsant mechanisms and neuroprotective effects of Mucuna pruriens (MP) seed in male BALB/c mice were evaluated. Ninety mice were kindled with picrotoxin, strychnine, or pilocarpine hydrochloride at the 30th minute of intraperitoneal injection (i.p) of normal saline (0.2 ml), MP (200, 100, 50 mg/kg), diazepam (7.5 mg/kg), or haloperidol (5 mg/kg). The onset of convulsion and percentage mortality was recorded. The histoarchitectural and immunohistochemical profiles of the brains were determined. Data were expressed as mean ± SEM with a one-way analysis of variance (ANOVA), while p < 0.05 was considered significant. There was a significant prolongation of the latency to first seizure across the treatment groups following picrotoxin, and pilocarpine-induced convulsion; a decrease in percentage mortality in the MP (50 mg/kg) treatment group, and an increase in the hippocampal nuclear factor erythroid 2-related factor 2 count, and Neu-N expression in the MP (200 mg/kg, and 100 mg/kg) treated mice. Treatment with MP seed may abolish seizure occurrence and consequential mortality; mechanisms traceable to its GABAergic expression and hippocampal NRF 2 and Neu N expression.