D-ribose-L-cysteine exhibits neuroprotective activity through inhibition of oxido-behavioral dysfunctions and modulated activities of neurotransmitters in the cerebellum of Juvenile mice exposed to ethanol.

Alcohol exposure to the cerebellum has been known to trigger cerebellar dysfunctions through several mechanisms. This present study was designed to evaluate the repealing effect of D-ribose-L-cysteine (DRLC) on alcohol-induced cerebellar dysfunctions in juvenile BALB/c mice. The animals were randomly divided into 4 groups (n = 10 per group). Mice were given oral administration of normal saline (control), DRLC (100 mg/kg, p.o), ethanol (0.2 mL of 10% w/v), or DRLC (100 mg/kg, p.o) + ethanol (0.2 mL of 10% w/v). On day 29 of the study (i.e., 24 h after the administration of the last respective doses), neurochemical quantification of the respective levels of serotonin and dopamine, lipid peroxidation, total antioxidant, superoxide dismutase, and glutathione peroxidase in the cerebellar tissues of the mice were analyzed. Compared with the saline-treated group, the studied neurochemical indices were modulated across the various experimental groups. The administration of ethanol significantly modulates the levels of monoamine neurotransmitters (serotonin and dopamine) as well as contents of total antioxidants, activities of superoxide dismutase, and glutathione peroxidase, with a concurrently increased level of lipid peroxidase in the cerebellar tissue of the mice. DRLC significantly reverses these effects in the DRLC + ethanol co-treated group. Combined exposure to DRLC + ethanol counteracts the deleterious effect of ethanol in the cerebellum of juvenile BALB/c mice via monoamine neurotransmitter, lipid peroxidation, total antioxidant status, superoxide dismutase, and glutathione peroxidase action pathways. Therefore, DRLC could be a pharmacologic or therapeutic agent in attenuating the deleterious effects of alcohol on the cerebellum.

Dexamethasone as endocrine disruptor; type I and type II (anti) oestrogenic actions on the ovary and uterus of adult Wistar rats (Rattus Novergicus).

OBJECTIVE: Dexamethasone is a widely used glucocorticoid, which has been prescribed increasingly in recent years. The effects of Dexamethasone on the ovary and uterus was investigated in present study. METHODS: Twenty (20) adult female Wistar rats, weighing 130-170 g were assigned to four (4) groups of five (5) animals each. The rats in the control group received saline, while the rats in the experimental group was subjected to oral treatment of dexamethasone of 12 mg/kg, 10 mg/kg, and 7 mg/kg doses daily for a period of 10 days, respectively. The rats were slaughtered after 24 hours of the last administration, and the uterus and ovaries were harvested following abdominal incision. Histological and biochemical investigations were carried out and the results were analyzed using ANOVA with the Graph-Pad prism software package 6. RESULTS: There was a significant decrease in the activities of the carbohydrate metabolic enzymes of the uterus in the dexamethasone-treated groups compared to the control group (p<0.05). Vacuolation, atrophy, thick epithelium, enlarged cells, inactive interstitial glands and follicular cyst, characterized the histological observation in the dexamethasone-treated groups in a dose-dependent manner. CONCLUSION: This present study revealed that high-dose dexamethasone causes multiple changes in the histological features of the ovary and uterus, exerting type I and type II anti-oestrogenic effects on the female reproductive compartment.

Morphine-alcohol treatment impairs cognitive functions and increases neuro-inflammatory responses in the medial prefrontal cortex of juvenile male rats / 대한해부학회지

In the developed and developing world, opioid consumption in combination with alcohol has become one of the substances abused. In this experiment, we examined the effects of alcohol, morphine, and morphine+alcohol combination on cognitive functions and neuroinflammatory responses in the medial prefrontal cortex (mPFC) of juvenile male rats. Alcohol (1.0 ml of 15% v/v ethanol twice daily, subcutaneously, 7 hours apart), morphine (0.5 ml/kg of 0.4 mg/kg morphine chlorate twice daily, subcutaneously, 7 hours apart), morphine+alcohol co-treatment (0.5 ml/kg of 0.4 mg/kg morphine chlorate+1.0 ml of 15% v/v ethanol twice daily, subcutaneously, 7 hours apart) were administered for 21 days. Treatment with morphine+alcohol significantly impairs cognition functions in the Morris water maze, passive avoidance, and novel object recognition tests, furthermore, the treatment significantly increased the quantitative count of astrocytic cells and also conferred marked neuronal cell death in the mPFC, which were studied by glial fibrillary acidic protein immunochemistry for astrocytes and Cresyl violet for Nissl's substance distribution in neurons respectively. These results suggest that alcohol, morphine, and morphine+alcohol co-treatment may trigger cognitive deficits and neuroinflammatory responses in the brain.