Evaluation of the Potential Neurotoxicity of Gold Nanoparticles in the Different Rat Brain Regions

The present study aims to investigate the potential adverse effects of gold nanoparticles (Au NPs) in the cortex, hippocampus, striatum, midbrain, cerebellum and medulla of adult male Wistar rat through the estimation of some oxidative stress parameters and acetylcholinesterase (AChE) activity. Rats were divided into two main experimental groups. Animals of the 1st and 2nd groups were intraperitoneally injected with a single dose (10

A Neurochemical and Electrophysiological Study on the Combined Effects of Caffeine and Nicotine in the Cortex of Rats

Introduction: Caffeine and nicotine are the most widely consumed psychostimulants worldwide. Although the effects of each drug alone on the central nervous system have been studied extensively, the literature on the neurochemical and electrophysiological effects of their combined treatments is scarce. The present study investigated the cortical electrophysiological and neurochemical alterations induced by acute administration of caffeine and nicotine in rats.  Methods: The rats received caffeine and nicotine at a 1-hour interval between the two treatments.  Results: Caffeine and nicotine administration resulted in a significant decrease in the concentrations of cortical amino acid neurotransmitters, namely glutamate, aspartate, glycine, and taurine, while γ-aminobutyric acid (GABA) significantly increased. Increased cortical lipid peroxidation and reduced glutathione and nitric oxide levels and acetylcholinesterase and Na⁺/K⁺-ATPase activities were also observed. The Electroencephalogram (EEG) showed an increase in delta frequency power band, whereas theta, beta-1, and beta-2 decreased after caffeine and nicotine treatment.  Conclusion: These findings suggest that caffeine and nicotine adversely exacerbate their stimulant effects manifested by the EEG changes mediated by increasing cholinergic transmission and disturbing the balance between the excitatory and inhibitory amino acids leading to oxidative stress

Nigella sativa as an anti-inflammatory and promising remyelinating agent in the cortex and hippocampus of experimental autoimmune encephalomyelitis-induced rats

Experimental autoimmune encephalomyelitis (EAE) is a well-established animal model of multiple sclerosis. This study aimed to investigate the protective and therapeutic effects of Nigella sativa (N. sativa) seeds (2.8 g/kg body weight) in EAE-induced rats. EAE-induced animals were divided into: (1) EAE-induced animals (“EAE” group). (2) “N. sativa + EAE” group received a daily oral administration of N. sativa 2 weeks prior to EAE induction until the end of the experiment. (3) “EAE + N. sativa” group received a daily oral administration of N. sativa after the appearance of the first clinical signs until the end of the experiment. All animals were sacrificed at the 28th day post EAE-induction. Disease pathogenesis was monitored using a daily clinical scoring, body weight, open field test, histopathological and ultrastructural examination and determination of some oxidative stress parameters in the cortex and hippocampus. N. sativa ameliorated the clinical signs and suppressed inflammation observed in EAE-induced rats. In addition, N. sativa enhanced remyelination in the hippocampus. However, protection of rats with N. sativa administered 2 weeks prior to EAE induction and its continuation until the end of the experiment resulted in a significant increase in the cortical lipid peroxide level with reference to control and “EAE” rats. In conclusion, N. sativa seeds could be used as a protective agent or an adjunct treatment for EAE even when the treatment started after the appearance of the first clinical signs. However, the dose and duration of N. sativa must be taken into consideration to avoid its probable pro-oxidant effect

Evaluation of the neuroprotective effect of taurine and green tea extract against oxidative stress induced by pilocarpine during status epilepticus

Status epilepticus (SE) has functional and structural consequences resulting in brain damage. The present study aims to investigate the role of taurine and green tea extract in the neuroprotection against oxidative stress and changes in acetylcholinesterase (AChE) and Na+,K+-ATPase activities during SE induced by pilocarpine in the hippocampus of adult male rats. Animals received an oral administration of either taurine (100 mg/kg) or green tea extract containing 100 mg/kg epigallocatechin gallate for 3 days before the induction of SE with pilocarpine (380 mg/kg, i.p.) and were sacrificed 1 h after pilocarpine injection. Data indicated that a state of oxidative stress has evolved during SE as evident from the significant increase in lipid peroxidation level and significant decrease in reduced glutathione (GSH) level. Significant decreases in AChE and Na+,K+-ATPase activities were also recorded. Pretreatment of rats with taurine exaggerated the increase in lipid peroxidation and failed to prevent the decrease in Na+,K+-ATPase activity resulting from pilocarpine. However, taurine pretreatment prevented the reduced activity of hippocampal AChE induced by pilocarpine during SE. Pretreatment of rats with green tea extract prevented the increase in lipid peroxidation occurring during SE. However, it failed to inhibit the decrease in Na+,K+-ATPase activity. In conclusion, taurine pretreatment failed to reduce the oxidative stress induced during SE. In contrast, pretreatment of rats with green tea extract ameliorated the oxidative stress induced by pilocarpine and this may assist in reducing the insults of hyperexcitability and excitotoxicity that occur during SE and thereby reduce neuronal damage