Berberine Supplement and Resistance Training May Ameliorate Diazinon Induced Neural Toxicity in Rat Hippocampus Via the Activation of the TrkB and ERK Signaling Pathway

Elham Shakouri, M. Azarbayjani, S. B. Jameie, M. Peeri, M. Farhadi
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引用次数: 2

Abstract

Background: Diazinon is an organophosphate pesticide that is broadly applied to control insectswhich causes oxidative damages in hippocampus tissue. We aimed to examine whether resistancetraining and berberine supplementation can protect the hippocampus against berberine-inducedneural toxicity.Methods: Fifty-six male Wistar rats were assigned randomly into eight groups of seven including:Control (Ctrl), Sham (normal saline), T1 (diazinon + berberine chloride (2 mg/kg) + resistancetraining), T2 (diazinon + berberine chloride [15 mg/kg] + resistance training), T3 (diazinon), T4(diazinon +resistance training), T5 (diazinon + berberine chloride [2 mg/kg]), and T6 (diazinon+ berberine chloride [15 mg/kg]). In the experimental groups, diazinon was intraperitoneallyadministered at a dose of 1.5 mg/kg. In the training groups, rats were trained every three days for sixweeks and 8-12 dynamic movements (repetitions) during each climb (six climbs for two sets). Theexpression of hippocampus PI3K and CDK genes and TrkB and ERK protein levels were evaluated inthe brain of diazinon-treated rats.Results: The protein expression of ERK and TrkB were increased following the treatment of diazinonintoxicated rats with berberine and resistance training (P=0.001). The administration of berberineat a dose of 15 mg/kg in combination with resistance training significantly (P=0.001) decreasedthe cell death rate in the hippocampus. Diazinon treatment caused extensive apoptosis in thehippocampus region of the rats’ brain (P=0.001). The gene expression of PI3K and CDK wassignificantly increased and the cell death rate significantly decreased (P=0.001) in the hippocampusfollowing the treatment of rats with berberine and resistance training.Conclusion: Six weeks of resistance training in combination with berberine treatment significantlyreduced apoptosis in the hippocampus region of diazinon-intoxicated rats. It seems theneuroprotection effects of berberine and resistance training are mediated by the stimulation of theexpression of enzymes responsible for the antioxidant defense within neuronal cells
补充小檗碱和抗阻训练可能通过激活TrkB和ERK信号通路改善重氮肼诱导的大鼠海马神经毒性
背景:二嗪农是一种有机磷农药,广泛应用于防治引起海马组织氧化损伤的昆虫。我们的目的是研究抗阻训练和补充小檗碱是否可以保护海马免受小檗碱诱导的神经毒性。方法:56只雄性Wistar大鼠随机分为8组,共7组:Control (Ctrl)、Sham(生理盐水)、T1(重氮嗪酮+小檗碱(2mg /kg) +阻力训练)、T2(重氮嗪酮+小檗碱[15mg /kg] +阻力训练)、T3(重氮嗪酮)、T4(重氮嗪酮+阻力训练)、T5(重氮嗪酮+小檗碱[2mg /kg])、T6(重氮嗪酮+小檗碱[15mg /kg])。实验组以1.5 mg/kg的剂量腹腔注射二嗪农。在训练组中,大鼠每三天训练一次,持续六周,每次攀登进行8-12次动态运动(重复)(两组6次攀登)。测定大鼠海马PI3K和CDK基因表达及TrkB和ERK蛋白水平。结果:双嗪嗪中毒大鼠经小檗碱和抗阻训练后,ERK和TrkB蛋白表达升高(P=0.001)。15 mg/kg剂量的小檗碱联合阻力训练显著降低海马细胞死亡率(P=0.001)。二嗪肼引起大鼠脑海马区广泛的细胞凋亡(P=0.001)。小檗碱加抗阻训练后大鼠海马PI3K和CDK基因表达显著升高,细胞死亡率显著降低(P=0.001)。结论:6周的抗阻训练联合小檗碱治疗可显著减少重嗪嗪中毒大鼠海马区的细胞凋亡。小檗碱和抗阻训练的神经保护作用似乎是通过刺激神经元细胞中负责抗氧化防御的酶的表达来调节的
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