Nigerian Psychoactive Alcoholic Herbal Mixture Impacts Behavioural Performance and Caused Brain Biochemical and Histopathological Alterations in Mice

Psychoactive alcoholic herbal mixture is popularly consumed because of the belief on its stimulant and curative effects. This study investigated the neurobehavioral, biochemical and histopathological consequences following its single and repeated co-administration with ethanol to mice. Mice were assessed for sensorimotor, anxiety and memory functions following acute and repeated administration of alcohol herbal mixture (AHM). Alterations in brain acetylcholineterase, nitrite, reduced glutathione (GSH) and malondialdehyde levels were assessed in striatum, prefrontal cortex (PFC) and hippocampus. Neuronal cells counts were determined in the prefrontal cortex and hippocampal tissues. In the acute study, AHM significantly impaired locomotor activity and motor coordination in mice. Repeated administration of AHM and AHM combined with ethanol caused significant impairment of locomotor and motor coordination, increased anxiety-like behavior and impaired memory in mice. Acetylcholinesterase activity was significantly increased in the PFC while nitrite level was elevated in the striatum and PFC. There was significant elevation of malondialdehyde and depletion of GSH in all brain regions as well as reduced neuronal cell counts in the PFC and hippocampus. This study showed evidences of behavioral perturbation and brain biochemical changes in mice, hence repeated consumption of alcoholic herbal mixture might produce substance-attributable harm and quicken neurodegenerative diseases in humans

Arjunolic acid counteracts fluoxetine-induced reproductive neuroendocrine dysfunction through inhibition of chromosomal derangements and hypercortisolism

Antidepression-related HPA-HPG alteration is gaining more attention in stress research on humans and animals with depression. Therefore, the search for therapeutic drugs such as Arjunolic acid (AA) might be a core value in the management of reproductive neuro-endocrine dysfuction in rats treated with FXT. In this context, this study aimed to determine the effects of AA on reproductive neuro-endocrine functions in fluoxetine (FXT)-induced HPA-HPG axis dysfunction in rats. The subjects were randomly divided into 6 groups with six (6) rats each after 14 days of acclimatization. Rats in group 1 received normal saline (10 mL/kg); groups 2 & 3 were respectively given AA (1.0 mg/100gm body weight) and AA (2.0 mg/100gm body weight), whereas rats in group 4 were given FXT (10 mg/kg/p.o./day), and groups 5 & 6 were respectively given a combination of FXT (10 mg/kg) + AA (1.0 mg/100g body weight) and of FXT (10 mg/kg) + AA (2.0 mg/100g body weight). The results revealed that FXT altered reproductive neuro-endocrine function as evidenced by increased corticosterone, tDFI, tCSA, and abnormal sperm morphology; with corresponding decreases in Kisspeptin, GnRH, LH, FSH, testosterone, HOST value, TP, Sialic acid, Johnson score, sperm count, motility, and viability. However, AA dose dependently significantly counteracted the FXT-elicited changes in corticosterone, tDFI, tCSA and abnormal sperm morphology as well as Kisspeptin, GnRH, LH, FSH, testosterone, HOST value, TP, Sialic acid, Johnson score, sperm count, motility, and viability; and improved the body and testicular weight in rats. In conclusion, AA attenuates fluoxetine-induced reproductive neuroendocrine dysfunction through inhibition of chromosomal derangements and hypercortisolism. However, co-administration of FXT with AA could be a better therapeutic option in the management of FXT-induced altered HPA-HPG-axis