Coenzyme Q10 attenuates neurodegeneration in the cerebellum induced by chronic exposure to tramadol

IF 2.7 4区 医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Majid Keyhanifard , Roghayeh Javan , Reza Ataee Disfani , Maryam Bahrami , Mohamad Sedigh Mirzaie , Saeid Taghiloo , Hossein Mokhtari , Davood Nasiry , Zahra Sadrzadeh Aghajani , Mahdi Shooraj
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引用次数: 0

Abstract

Background

Chronic use of tramadol can cause neurotoxic effects and subsequently cause neurodegeneration in the cerebellum. The main damage mechanisms identified are oxidative stress and inflammation. Currently, we investigated the effects of coenzyme Q10 (CoQ10) in attenuates of neurodegeneration in the cerebellum induced by chronic exposure to tramadol.

Material and methods

Seventy-two male mature albino rats were allocated into four equal groups, including; non-treated group, CoQ10 group (which received CoQ10 at 200 mg/kg/day orally for three weeks), tramadol group (which received tramadol hydrochloride at 50 mg/kg/day orally for three weeks), and tramadol+CoQ10 group (which received tramadol and CoQ10 at the same doses as the previous groups). Tissue samples were obtained for stereological, immunohistochemical, biochemical, and molecular evaluations. Also, functional tests were performed to evaluate behavioral properties.

Results

We found a significant increase in stereological parameters, antioxidant factors (catalase, glutathione, and superoxide dismutase), and behavioral function scores in the tramadol+CoQ10 group compared to the tramadol group (p < 0.05). In addition, malondialdehyde levels, the density of apoptotic cells, as well as the expression of pro-inflammatory (tumor necrosis factor-alpha, interleukin 1 beta, and interleukin 6) and autophagy (lysosome-associated membrane protein 2, autophagy-related 5, beclin 1, and autophagy-related 12) genes were considerably reduced in the tramadol+CoQ10 group compared to the tramadol group (p < 0.05).

Conclusion

We conclude that the administration of CoQ10 has neuroprotective effects in the cerebellum of rats that have chronic exposure to tramadol.

Abstract Image

辅酶Q10减轻慢性曲马多引起的小脑神经退行性变。
背景:长期使用曲马多可引起神经毒性作用,随后引起小脑神经退行性变。确定的主要损伤机制是氧化应激和炎症。目前,我们研究了辅酶Q10 (CoQ10)在慢性曲马多诱导的小脑神经退行性变中的作用。材料与方法:雄性成年白化大鼠72只,随机分为4组:未治疗组,辅酶q10组(口服辅酶q10 200mg/kg/天,持续三周),曲马多组(口服盐酸曲马多50mg/kg/天,持续三周),曲马多+辅酶q10组(曲马多和辅酶q10的剂量与前几组相同)。获得组织样本进行体视学、免疫组织化学、生化和分子评价。此外,还进行了功能测试以评估行为特性。结果:我们发现,与曲马多组相比,曲马多+辅酶q10组的体视学参数、抗氧化因子(过氧化氢酶、谷胱甘肽和超氧化物歧化酶)和行为功能评分显著增加(p结论:我们得出结论,慢性暴露于曲马多的大鼠的小脑中给予辅酶q10具有神经保护作用。
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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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