Ganoderma lucidum ethanol extract promotes weight loss and improves depressive-like behaviors in male and female Swiss mice.

Metabolic and mood-related disturbances can increase the risks of developing adverse mental health problems. The medicinal mushroom, Ganoderma lucidum, is utilized in indigenous medicine to improve quality of life, promote health, and boost vitality. This study investigated the effects of Ganoderma lucidum ethanol extract (EEGL) on feeding behavioral parameters, depressive-like symptoms, and motor activity in Swiss mice. We hypothesized that EEGL would have beneficial effect on metabolic and behavioral outcomes in a dose-related manner. The mushroom was identified and authenticated via techniques of molecular biology. Forty Swiss mice (n = 10/group) of either sex were given distilled water (10 mL/kg) and graded doses of EEGL (100, 200, and 400 mg/kg) orally for 30 days, during which feed and water intake, body weight, neurobehavioral, and safety data were documented. The animals experienced a significant decrease in body weight gain and feed intake while water intake increased in a dose-dependent manner. Furthermore, EEGL significantly diminished immobility time in forced swim test (FST) and tail suspension test (TST). At the 100 and 200 mg/kg, EEGL did not cause significant alteration in motor activity in the open field test (OFT). Meanwhile, an increase in motor activity in male mice without remarkable difference in female mice was observed at the highest dose (400 mg/kg). Eighty percent of mice treated with 400 mg/kg survived till day 30. These findings suggest that EEGL at 100 and 200 mg/kg reduces the amount of weight gained and elicits antidepressant-like effects. Thus, EEGL might be useful for the management of obesity and depressive-like symptoms.

Pretreatment with Carpolobia lutea ethanol extract prevents schizophrenia-like behavior in mice models of psychosis.

ETHNOPHARMACOLOGICAL RELEVANCE: Carpolobia lutea decoction is widely used as a phytotherapeutic against central nervous system-related disorders including insomnia, migraine headache, and mental illness in West and Central Tropical Africa. AIM: This study was designed to investigate the antipsychotic activity of Carpolobia lutea (EECL) in mice models of psychosis. METHODS: Male Swiss mice (n = 5/group) were given EECL (100, 200, 400, and 800 mg/kg), haloperidol (1 mg/kg), clozapine (5 mg/kg) and vehicle (10 mL/kg) orally before amphetamine (5 mg/kg)-induced hyperlocomotion and stereotypy, apomorphine (2 mg/kg)-induced stereotypy, or ketamine (10, 30, and 100 mg/kg)-induced hyperlocomotion, enhancement of immobility and cognitive impairment. RESULTS: EECL (200, 400, and 800 mg/kg) prevented amphetamine- and apomorphine-induced stereotypies, as well as reduced hyperlocomotion induced by amphetamine and ketamine, all of which are predictors of positive symptoms. Regardless of the dose administered, EECL prevented the index of negative symptoms induced by ketamine. Furthermore, higher doses of EECL (400 and 800 mg/kg) also prevented ketamine-induced cognitive impairment, a behavioral phenotype of cognitive symptoms. CONCLUSION: Pretreatment with EECL demonstrated antipsychotic activity in mice, preventing amphetamine-, apomorphine-, and ketamine-induced schizophrenia-like symptoms, with 800 mg/kg being the most effective dose.

Melatonin salvages lead-induced neuro-cognitive shutdown, anxiety, and depressive-like symptoms via oxido-inflammatory and cholinergic mechanisms.

INTRODUCTION: Lead is the most used nonphysiological neurotoxic heavy metal in the world that has been indicated to interfere with the cognitive and noncognitive processes via numerous mechanisms. The neuroprotective effect of melatonin is well known, but the effect of its interaction with lead in the brain remains inconclusive. OBJECTIVE: To assess the therapeutic role of melatonin on cognitive deficit, anxiety and depressive-like symptoms in matured male Wistar rats exposed to a subchronic lead chloride (PbCl2 ). METHODS: Twenty male Wistar rats were blindly randomized into four groups (n = 5/group): group 1 to 4 underwent intragastric administration of physiological saline (10 ml/kg; vehicle), PbCl2 (50 mg/kg), melatonin (10 mg/kg) and PbCl2 + melatonin respectively for a period of 4 weeks during which neurobehavioral data were extracted, followed by neurochemical and histopathological evaluations. RESULTS: Exposure to PbCl2 reduced cognitive performance by increasing the escape latency and average proximity to the platform zone border, decreasing average path length in the platform zone, cognitive score, and time spent in probing. It raised the thigmotaxis percentage, time spent in rearing, number of pellet-like feces, and time spent in the dark compartment of a bright/dark box which are predictors of anxiety. It also induced depressive-like behavior as immobility time was enhanced. PbCl2 deranged neurochemicals; malondialdehyde, interlukin-1ß, and tumor necrotic factor-α were increased while superoxide dismutase and acetylcholinesterase were decreased without remarkable alteration in reduced glutathione and nitric oxide. Administration of PbCl2 further disrupted neuronal settings of hippocampal proper and dentate gyrus. In contrast, the supplementation of melatonin reversed all the neurological consequences of PbCl2 neurotoxicity by eliciting its properties against oxidative and nonoxidative action of PbCl2 . CONCLUSION: These findings suggest that melatonin down-regulates neurotoxicant interplays in the brain systems. Therefore, this study suggests the use of melatonin as an adjuvant therapy in neuropathological disorders/dysfunctions.