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Alcohol‐induced aggression and related violence is a serious and common social problem globally. Alcohol use is increasingly found in the form of alcoholic herbal mixtures (AHM) with indiscriminate and unregulated alcohol content. This study investigated the effects of AHM on aggressive‐like, neurocognitive impairment and brain biochemical alteration in mice. Thirty‐two male resident mice were paired housed with female mice for 21 days in four groups (n = 8). Resident mice were treated orally with normal saline, AHM, ethanol and AHM + ethanol daily for 14 days. Aggressive‐like behaviour was scored based on the latency and frequency of attacks by the resident mouse on the intruder. Neurocognitive impairment was determined using the Y‐maze test (YMT) and novel object recognition test (NORT). Acetylcholinesterase, glutamic acid decarboxylase (GAD), pro‐inflammatory and oxidative stress parameters were determined in the prefrontal cortex (PFC). Neuronal morphology, cytochrome c (Cyt‐c) and nuclear factor‐kappa B (NF‐ĸB) expressions were determined. AHM and in combination with ethanol showed an increased index of aggression typified by frequency of attack and reduced latency to attack when compared to normal saline‐treated animals. Co‐administration of AHM and ethanol significantly reduced cognitive correct alternation (%) and discrimination index in the YMT and NORT, respectively. AHM and ethanol increased acetylcholinesterase, Pro‐inflammatory cytokines and oxidative stress parameters while they reduced GAD. There were significantly reduced neuronal counts and increased expression of Cyt‐c and NF‐ĸB, respectively Alcoholic herbal mixture increased aggressiveness and caused neurocognitive impairment via increased oxido‐inflammatory stress in the prefrontal cortex. [ABSTRACT FROM AUTHOR]

The leaves of Clerodendrum polycephalum Baker (Labiatae) are used as a dietary legume supplement and applied ethnomedicinally for the management of epilepsy, convulsion, and spasms. This study is aimed at evaluating the effects of Clerodendrum polycephalum (CP) leaf extract on chemical‐induced seizures in mice and the possible mechanisms of action. Swiss albino mice were pretreated with CP (50, 100, or 500 mg/kg, p.o.) prior to intraperitoneal injection of picrotoxin (PTX) or pentylenetetrazole (PTZ). However, the most effective dose was used to elucidate the role of GABAergic and nitric oxide‐cyclic guanosine monophosphate (NO‐cGMP) signaling mechanisms in mice brains. Accordingly, we evaluated the preventive and reversal effects of CP on kainic acid (KA)‐induced temporal lobe epilepsy (TLE), oxidative stress, and neuroinflammatory in mice. The pretreatment of mice with CP delayed the latencies to PTX and PTZ‐induced seizures and decrement in the period of tonic–clonic attacks. Interestingly, CP (100 mg/kg) completely prevented PTZ‐induced tonic–clonic seizures. Contrastingly, flumazenil (benzodiazepine receptor antagonist), NG‐nitro‐L‐Arginine (L‐NNA) (10 mg/kg., neuronal nitric oxide synthase inhibitor), and methylene blue (MB) (2 mg/kg, a soluble guanylyl cyclase inhibitor) but not L‐arginine (150 mg/kg., nitric oxide precursor) reversed CP‐induced anticonvulsant‐like effect in PTZ model. Furthermore, KA‐elicited TLE was prevented by CP treatment. CP also attenuated KA‐induced oxidative stress, cyooxygenase‐2 (COX‐2), and nuclear factor kappa‐B (NF‐κB) elevated expressions in the hippocampus. The study revealed that the ethanolic leaf extract of CP produced anticonvulsant actions through enhancement of antioxidant defense, GABAergic, and NO‐cGMP signaling pathways as well as attenuation of inflammatory processes. Practical applications: The leaves of Clerodendrum polycephalum Baker (Labiatae) are used as a dietary legume supplement and applied ethnomedicinally for the management of epilepsy, convulsion, and spasms. For this reason, we believe that supplementation of the Clerodendrum polycephalum leaf extract would prevent epileptic‐related disorders in mice induced with epileptic conditions using kainic acid and other behavioral phenotypic models. Here, our findings clearly revealed that Clerodendrum polycephalum leaf extract protects against conditions of epileptic‐related disorders and thus might be relevant as a dietary supplement in the prevention or delay of the onset of seizures and epileptic behavior. [ABSTRACT FROM AUTHOR]

d‐Ribose‐l‐cysteine (DRLC) is an analogue of cysteine that has been shown to boost cellular antioxidant capacity by enhancing intracellular biosynthesis of glutathione (GSH). Deficiency of GSH has been implicated in the pathogenesis of Alzheimer's disease (AD), a neurodegenerative disorder associated with loss of memory. Thus, the use of antioxidants to prevent or retard the progression of memory deteriorations in persons with AD has been the focus of intense investigations. This study was carried out to evaluate the effects of DRLC on memory and scopolamine‐induced amnesia, acetyl‐cholinesterase activity, and oxidative stress in mice. Male Swiss mice were given oral administration of saline (10 ml/kg), DRLC (25, 50, and 100 mg/kg) or donepezil (1 mg/kg) 30 min before testing for memory performance using Y‐maze and object recognition models. Another set of mice were also pretreated orally with saline, DRLC (25, 50, and 100 mg/kg) or donepezil (1 mg/kg) but in combination with scopolamine (3 mg/kg, i.p.) daily for 7 days. Thirty minutes after treatment on Day 7, memory function was then evaluated. The brain levels of acetyl‐cholinesterase and oxidative stress parameters were assayed. DRLC significantly (p <.05) enhanced memory performance and attenuated scopolamine‐induced amnesia. Increased acetyl‐cholinesterase activity and oxidative stress, as shown by decreased antioxidant substrates (glutathione and catalase) and elevated malondialdehyde contents in mice with scopolamine amnesia were also attenuated by DRLC. Our findings suggest that inhibition of oxidative stress and acetyl‐cholinesterase activity might contribute to the potential benefit of DRLC in persons with amnesia. [ABSTRACT FROM AUTHOR]

l‐Arginine‐nitric oxide pathway has been reported to be involved in the mediation of the psychopharmacological effects of many psychotropic drugs. Previous studies have shown that morin, a psychotropic compound isolated from mulberry leaf produces functional psychopharmacological effects indicative of antidepressant, antipsychotic, anxiolytic and nootropic properties. However, the role of l‐arginine‐nitric oxide pathway in the psychotropic effects of morin has not been fully investigated, hence, the need for this study. Male Swiss mice were pretreated individually or in combination with nitric oxide precursor [l‐arginine (750 mg/kg, i.p.)], competitive nonselective nitric oxide synthase (NOS) inhibitor [N(G)‐nitro‐l‐arginine methyl ester (l‐NAME, i.p) (50 mg/kg)] or selective neuronal NOS inhibitor [methylene blue (3.75 mg/kg, i.p)] prior to morin (100 mg/kg, i.p.) or saline (10 mL/kg, i.p.) treatment. Psychopharmacological activities were then evaluated 30 min later using open field, Y‐maze, and forced swim tests. l‐Arginine significantly reversed the effects of morin on locomotion, memory and depression in mice. The reduced motor activity and enhanced memory function produced by morin were significantly attenuated by methylene blue but augmented the antimobility activity of morin in the FST. Moreover, l‐NAME potentiated the psychopharmacological effects of morin in the open field and forced swim tests but reduced its memory promoting effect. Meanwhile, morin supplementation reversed the effects of l‐arginine on l‐NAME‐treated mice in all behavioral models. The results of this study suggest that l‐arginine‐nitric oxide pathway might play a role in the modulation of the antidepressant and memory promoting effects of morin in mice. [ABSTRACT FROM AUTHOR]

Abstract: The antidepressant‐like activity of ethanol seed extract of Aframomum melegueta (AM) in mice was evaluated in this study. The duration of immobility was measured 30 min after oral administration of AM (25–400 mg/kg) in forced swim test. In the unpredictable chronic mild stress (UCMS) paradigm, mice were treated with AM (25–100 mg/kg) 30 min before exposure to different stressors for 14 days. Thereafter, sucrose preference test, tail suspension test, and test for anxiety were done. The brain concentrations of malondialdehyde and glutathione were estimated spectrophotometrically. Brain histology and population of healthy neurons in cornu ammonis 3 of the hippocampus were also assessed. AM (25 and 50 mg/kg) significantly decreased the duration of immobility in forced swim test and prevented UCMS‐induced anhedonia and anxiety‐like behaviors, suggesting antidepressant potentials. The extract decreased malondialdehyde and increased glutathione concentrations in UCMS‐induced mice. Therefore, AM extract offers protection against UCMS‐induced damage to cornu ammonis 3 hippocampal neuronal cells indicating neuroprotection. Practical applications: The seed of Grains of Paradise (Aframomum melegueta) is used in traditional medicine for fatigue and impotence, which are prominent symptoms of major depression. It is also widely chewed for its presumed central nervous system stimulant and endurance promoting effects. The results of this study revealed valuable evidence concerning the possible use of Grains of Paradise as an affordable natural, alternative, and/or complementary therapy with antioxidative and neuroprotective potentials. Consumption of these seeds in the right quantity might provide health benefits as Grains of Paradise exhibited antidepressant‐like effect via inhibition of oxidative stress and neuroprotection. [ABSTRACT FROM AUTHOR]

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