10-dehydrogingerdione amends tramadol-elicited neurotransmitters disturbance and apoptosis in the brain of male rats by repleting non-enzymatic antioxidants

IF 2.7 4区 医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Mohamed M. ELseweidy , Sousou I. Ali , Laila Sabik , Salma E. Sewilam
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引用次数: 0

Abstract

Tramadol is analgesic medication to relief acute and chronic pain, referred to as alternative to opioid drugs however its abuse or overdosage may resulted in neuronal toxicity. This is attributed to severe fluctuations of neurotransmitters pattern along with cerebral inflammation and oxidative damage. Present work was undertaken to illustrate the cytoprotective effect of 10-dehydrogingerdione (10-DHGD) on the brain tissues of experimental rats due to Tramadol intake and its underlying mechanism. 24 male wistar rats were randomized into 4 equal groups. Group (1), received tramadol in a dose level 20 mg/kg intrapertioneal (i.p) daily for 30 days and referred to Tramadol group. Group (2), received both of 10-DHGD (10 mg/kg, orally) one hour before tramadol intake (dose as mentioned before) daily for 30 days. Group (3) received 10-DHGD only (10 mg/kg, orally) and daily for 30 days. Group (4), received no drugs and referred to control group for comparison. Tramadol significantly reduced Norepinephrin (NE), dopamine, serotonin and glutathione (reduced) contents of Cerebral cortex. lipid peroxidation, nuclear factor kappa B (NFkB), inducible nitric oxide synthase (INOS) levels and caspase-3 immunoreactivity showed however significant increase. Of note, 10-DHGD significantly increased neurotransmitters, glutathione contents while Malondialdehyde (MDA), Nitric oxide (NO), NFkB, INOS additionally caspase-3 immunoexpression showed significant decrease i.e counteracted to certain extent tramadol effect. These findings may refer to the cytoprotective potential of 10-DHGD against the neurotoxicity exerted by tramadol intake, most probably mediated via enhancement of endogenous antioxidants system.

10-脱氢姜二酮通过补充非酶抗氧化剂改善曲马多诱导的雄性大鼠脑内神经递质紊乱和细胞凋亡
曲马多是一种缓解急性和慢性疼痛的镇痛药物,被称为阿片类药物的替代品,但其滥用或过量使用可能导致神经元毒性。这归因于神经递质模式的严重波动以及大脑炎症和氧化损伤。本工作旨在阐明10-脱氢姜二酮(10-DHGD)因摄入曲马多而对实验大鼠脑组织的细胞保护作用及其潜在机制。24只雄性wistar大鼠随机分为4组。第(1)组,每天腹膜内(i.p)接受剂量水平为20mg/kg的曲马多,持续30天,并参考曲马多组。第(2)组,在每天摄入曲马多(剂量如上所述)前1小时接受10-DHGD(10 mg/kg,口服),持续30天。组(3)仅接受10-DHGD(10 mg/kg,口服),并每天持续30天。第(4)组,未接受任何药物治疗,并将其转诊至对照组进行比较。曲马多显著降低大脑皮层去甲肾上腺素(NE)、多巴胺、血清素和谷胱甘肽(减少)的含量。脂质过氧化、核因子κB(NFkB)、诱导型一氧化氮合酶(INOS)水平和胱天蛋白酶-3免疫反应活性均显著升高。值得注意的是,10-DHGD显著增加了神经递质、谷胱甘肽含量,而丙二醛(MDA)、一氧化氮(NO)、NFkB、INOS另外的胱天蛋白酶-3免疫表达显著降低,即在一定程度上抵消了曲马多的作用。这些发现可能涉及10-DHGD对曲马多摄入产生的神经毒性的细胞保护潜力,这很可能是通过增强内源性抗氧化剂系统介导的。
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来源期刊
Journal of chemical neuroanatomy
Journal of chemical neuroanatomy 医学-神经科学
CiteScore
4.50
自引率
3.60%
发文量
87
审稿时长
62 days
期刊介绍: The Journal of Chemical Neuroanatomy publishes scientific reports relating the functional and biochemical aspects of the nervous system with its microanatomical organization. The scope of the journal concentrates on reports which combine microanatomical, biochemical, pharmacological and behavioural approaches. Papers should offer original data correlating the morphology of the nervous system (the brain and spinal cord in particular) with its biochemistry. The Journal of Chemical Neuroanatomy is particularly interested in publishing important studies performed with up-to-date methodology utilizing sensitive chemical microassays, hybridoma technology, immunocytochemistry, in situ hybridization and receptor radioautography, to name a few examples. The Journal of Chemical Neuroanatomy is the natural vehicle for integrated studies utilizing these approaches. The articles will be selected by the editorial board and invited reviewers on the basis of their excellence and potential contribution to this field of neurosciences. Both in vivo and in vitro integrated studies in chemical neuroanatomy are appropriate subjects of interest to the journal. These studies should relate only to vertebrate species with particular emphasis on the mammalian and primate nervous systems.
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