The current objective is to evaluate the effect of frankincense oil on the convulsions and the associated neurochemical alterations produced in pilocarpine-induced status epilepticus rat model. Rats were divided randomly into: control, status epilepticus rat model and rat model of status epilepticus pretreated with frankincense oil daily for 5 days before pilocarpine treatment. On the fifth day, after pilocarpine injection, rats were observed to evaluate the severity of seizures for 2 h. The oxidative stress parameters malondialdehyde, reduced glutathione and nitric oxide, the proinflammatory cytokines interleukin-6 and interleukin-1β and acetylcholinesterase were determined in the cortex, hippocampus and striatum. Dopamine, norepinephrine and serotonin were measured in the cortex and striatum. The status epilepticus model exhibited repetitive seizures in the form of generalized tonic- clonic convulsions after 30 min. of pilocarpine injection. This was associated with a significant increase in the levels of malondialdehyde and nitric oxide and a significant decrease in reduced glutathione in the three regions. A significant increase was also observed in interleukin-1β, interleukin-6 and acetylcholinesterase. In the cortex and striatum, a significant decrease was recorded in monoamine levels. Pretreatment of rat model of status epilepticus with frankincense oil decreased the severity of seizures that appeared in the form of tremors and facial automatisms and prevented the increase in malondialdehyde, nitric oxide, interleukin-1β, interleukin-6 and acetylcholinesterase and the decrease in reduced glutathione induced by pilocarpine in the studied brain regions. Frankincense oil failed to restore the decreased level of cortical serotonin and dopamine. In the striatum, frankincense oil improved the levels of serotonin and norepinephrine but failed to restore the decreased dopamine levels. It is clear from the present results that frankincense oil reduced the severity of seizures induced by pilocarpine. This could be mediated by its potent antioxidant and anti-inflammatory effects.

中文翻译：

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乳香油对癫痫持续状态大鼠神经化学变化的影响

当前的目的是评估乳香油对毛果芸香碱引起的癫痫持续状态大鼠模型中惊厥和相关神经化学变化的影响。将大鼠随机分为：对照组，癫痫持续状态大鼠模型和每天在毛果芸香碱治疗前用乳香油预处理5天的癫痫持续状态大鼠模型。在注射毛果芸香碱后的第五天，观察大鼠评估癫痫发作的严重程度，持续2小时。测定皮层，海马和纹状体中的氧化应激参数丙二醛，还原型谷胱甘肽和一氧化氮，促炎细胞因子白细胞介素6和白细胞介素1β和乙酰胆碱酯酶。在皮质和纹状体中测量多巴胺，去甲肾上腺素和5-羟色胺。癫痫持续状态模型在30分钟后表现出以强直性阵挛性抽搐形式反复发作。毛果芸香碱注射液。这与这三个区域中丙二醛和一氧化氮水平的显着增加以及还原型谷胱甘肽的显着降低有关。在白介素-1β，白介素-6和乙酰胆碱酯酶中也观察到显着增加。在皮层和纹状体中，单胺水平明显下降。用乳香油预处理癫痫持续状态大鼠模型可降低以震颤和面部自发性发作形式出现的癫痫发作的严重程度，并防止丙二醛，一氧化氮，白介素-1β的升高，在研究的脑区域中，白介素6和乙酰胆碱酯酶以及毛果芸香碱引起的还原型谷胱甘肽减少的减少。乳香油未能恢复皮质5-羟色胺和多巴胺水平的降低。在纹状体中，乳香油改善了5-羟色胺和去甲肾上腺素的水平，但未能恢复降低的多巴胺水平。从目前的结果可以明显看出，乳香油降低了毛果芸香碱引起的癫痫发作的严重程度。这可以通过其有效的抗氧化剂和抗炎作用来介导。从目前的结果可以明显看出，乳香油降低了毛果芸香碱引起的癫痫发作的严重程度。这可以通过其有效的抗氧化剂和抗炎作用来介导。从目前的结果可以明显看出，乳香油降低了毛果芸香碱引起的癫痫发作的严重程度。这可以通过其有效的抗氧化剂和抗炎作用来介导。