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首页> 外文期刊>Cytokine >The protective effect of rifampicin on behavioral deficits, biochemical, and neuropathological changes in a cuprizone model of demyelination
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The protective effect of rifampicin on behavioral deficits, biochemical, and neuropathological changes in a cuprizone model of demyelination

机译：利福平对脱髓鞘铜苏酮模型的行为缺陷，生化和神经病理变化的保护作用

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摘要

Multiple sclerosis (MS) is a disease of the central nervous system (CNS) in which both neuroinflammation and neurodegeneration play critical roles in the pathogenesis of the disease. A growing body of evidence indicates that some antibiotics have anti-inflammatory and neuroprotective properties. Rifampicin, commonly used for the treatment of mycobacteria, has been shown to exert neuroprotective activities in neurodegenerative diseases. In this study, we examined the efficacy of rifampicin on demyelination, gliosis, apoptosis, inflammation, behavioral dysfunction, and biochemical alterations in the cuprizone model of demyelination. For this aim, male C57BL/6J mice were fed a chow containing 0.2% cuprizone (w/w) for 6 weeks to induce reversible demyelination in the corpus callosum. Mice intraperitoneally received serial doses of rifampicin (10, 20, or 40 mg/kg body weight) in the last 7 days of a 6-week period of cuprizone treatment. The results showed that the administration of rifampicin led to the improvement in motor behavioral deficits. In line with this, rifampicin decreased the number of apoptotic cells in the corpus callosum thereby diminishing the expression of cleaved caspase-3 and Bax, as well as increasing Bcl-2. Moreover, rifampicin significantly lowered the levels of interleukin-6, interleukin-1 beta, caspase-12 activity, heme oxygenase-1(HO-1), nitric oxide (NO), and malondialdehyde (MDA) in mice treated with cuprizone. Conversely, the activity of glutathione peroxidase (GPx) and the level of ferric reducing ability of plasma (FRAP) were increased in response to the treatment with rifampicin. Histopathological findings demonstrated that rifampicin statistically promoted remyelination and mitigated microgliosis and astrogliosis. It seems that rifampicin is able to be added to the armamentarium of therapies for multiple sclerosis.
机译：多发性硬化症（MS）是中枢神经系统（CNS）的疾病，其中神经炎症和神经变性都在疾病的发病机制中发挥着关键作用。越来越多的证据表明一些抗生素具有抗炎和神经保护性能。已经显示出常用于治疗分枝杆菌的利福平素，在神经变性疾病中发挥神经保护活性。在这项研究中，我们研究了利福平在脱髓鞘的Cuprizone模型中对脱髓鞘，渗透性，凋亡，炎症，行为功能障碍和生物化学改变的疗效。为此目的，将雄性C57BL / 6J小鼠送入含有0.2％铜酮（W / W）的含量6周，以诱导胼callosum中的可逆脱髓鞘。在铜沸酮治疗的6周期期间，腹膜内腹腔内接受连续的利福平（10,20，或40mg / kg体重）的连续剂量。结果表明，利福平给药导致电机行为缺陷的改善。符合此，利福平降低了胼callosom中的凋亡细胞的数量，从而降低切割的Caspase-3和Bax的表达，以及增加的Bcl-2。此外，利福平显着降低了白细胞介素-6，白细胞介素-1β，Caspase-12活性，血红素氧基酶-1（HO-1），一氧化氮（NO）和用铜金属化合物的丙醛（MDA）。相反，谷胱甘肽过氧化物酶（GPX）的活性和血浆（FRAP）的降低能力水平响应于利福平的治疗而增加。组织病理学发现表明，利福平促进了重新髓鞘化和缓解的微细胞源症和星分激。似乎利福平能够添加到多发性硬化的疗法的疗法中。

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