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

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

The potential role of pumpkin seeds oil on methotrexate-induced lung toxicity

Abstract Many chemotherapeutic drugs cause adverse pulmonary reactions leading to severe pulmonary disease. Though methotrexate (MTX) is used for the treatment of cancer and other diseases, it is highly toxic with multiple adverse effects including pulmonary toxicity. Essential oils represent an open frontier for pharmaceutical sciences due to their wide range of pharmacological properties. Pumpkin seeds oil (PSO) was used to investigate its ability to alleviate methotrexate-induced lung toxicity in rats. Lung tissue from MTX-treated group revealed a decrease in malondialdehyde, glutathione, and nitric oxide accompanied by a marked inhibition in cholinesterase activity, and enhanced catalase activity, tumor necrosis factor-α, interleukin-6 and vascular endothelial growth factor levels. Analysis of PSO revealed that the oil was rich in hexadecanoic acid, decane methyl esters, squalene, polydecane, docosane, and other derivatives. Administration of PSO ameliorated the oxidant/antioxidant and proinflammatory changes induced by MTX in the lung tissue. Histological examinations confirmed the potency of PSO in reducing the histopathological alterations induced by MTX. Immunohistochemical analysis showed decreased nuclear factor-kappa B and caspase 3 expression after PSO. The present data indicated the protective efficiency of PSO against MTX-induced lung injury by decreasing oxidative damage, inflammation and apoptosis and could thus be recommended as an adjuvant therapy