多发性硬化(MS)对中枢神经系统(CNS)的影响

A. Ahmadi
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引用次数: 0

摘要

多发性硬化症(MS)是一种中枢神经系统自身免疫性疾病,髓磷脂成分被免疫系统特异性靶向,导致髓磷脂轴突破坏和相关衰弱症状[1-3]。此外,根据研究,没有发现有效的治疗这种疾病的方法。因此,需要一种安全有效的多发性硬化症治疗方案。此外,中枢神经系统(CNS)被血脑屏障与免疫系统分离,传统上被认为是“免疫系统保护”,免疫细胞也能够靶向大脑,导致CNS自身免疫性疾病Pahan等[4]。一篇测量肉桂对多发性硬化症小鼠影响的文章使用了肉桂和肉桂树的棕色树皮,肉桂树在世界各地被用作香料或调味品已有几个世纪了。此外,中世纪的医生将肉桂用于医疗目的,以治疗各种疾病,如骨关节炎、咳嗽、声音嘶哑、喉咙痛等。此外,根据各种文献的发现,结果表明广泛的炎症,调节性T细胞(Tregs)的丧失,自身免疫Th1和Th17细胞的过度活跃,脑血脑屏障(BBB)和血脊髓屏障(BSB)的衰竭,以及CNS中光保护分子的丧失是MS需要的一些症状[1-3]。有趣的是,NaB处理能够抑制培养的星形胶质细胞和小胶质细胞中促炎分子的表达[4]。甲羟戊酸、3-羟基-3甲基戊二酰辅酶A和焦磷酸法尼酯(甲羟戊二酸途径的介质)通过抑制NF-κB的活化和一氧化氮合酶(iNOS)的表达逆转NaB。它通过抑制胆固醇生物合成途径具有炎症作用。然而,尽管NaB能够降低胆固醇水平,但胆固醇对nabb介导的iNOS没有抑制作用[4]。Brahmachari等[4]在一篇文章中,他们测量了肉桂对MS小鼠的影响,其中NaB通过降低p21ras的激活来降低胶质细胞中NF-κB的激活和iNOS的表达,根据口服肉桂粉[5]和含有NaB代谢物[4]的饮用水可抑制EAE小鼠脊髓和小脑中iNOS和IL-1β的体内表达。这些发现表明肉桂能够减少大鼠中枢神经系统的体内炎症,EAE也是神经退行性疾病如阿尔茨海默病(AD)和帕金森病(PD),肉桂和NaB的另一个特征。它还能改善阿尔茨海默病动物模型[6]和黑纹状体的海马功能。动物模型PD保护[7]。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Effect of Multiple Sclerosis (MS) on Central Nervous System (CNS)
Multiple sclerosis (MS) is an autoimmune disorder of the CNS in which myelin components are specifically targeted by the immune system and lead to the destruction of myelin axons and associated debilitating symptoms [1-3]. Also, according to studies, no effective treatment for this disease has been found. Therefore, a safe and effective treatment option for MS is needed. Also, the central nervous system (CNS) is separated from the immune system by a blood-brain barrier and is traditionally considered “immune system protection”, and immune cells are also able to target the brain and lead to CNS autoimmune disorders Pahan et al. [4]. An article measuring the effects of cinnamon on MS mice used cinnamon and the brown bark of the cinnamon tree, which has been used as a spice or flavoring around the world for centuries. In addition, medieval physicians used cinnamon for medical purposes to treat a variety of disorders such as osteoarthritis, cough, hoarseness, sore throat, etc. Also, according to the findings of various articles, the results show that widespread inflammation, Loss of regulatory T cells (Tregs), autoimmune Th1 and Th17 cell hyperactivity, failure of the cerebral blood-brain barrier (BBB) and blood-spinal cord barrier (BSB), and loss of light-protective molecules in the CNS are some of the symptoms that Demystifying manifestations are required in MS [1-3]. Interestingly, NaB treatment is able to inhibit the expression of proinflammatory molecules in cultured astrocytes and microglia [4]. Reversal of NaB by inhibiting NF-κB activation and expression of nitric oxide synthase (iNOS) by mevalonate, 3-hydroxy-3methylglutaryl-coenzyme A and farnesyl pyrophosphate, mediators of the mevalonate pathway, in active astrocytes suggests that NaB. It has an inflammatory effect by inhibiting the cholesterolbiosynthesis pathway However, although NaB is able to lower cholesterol levels, cholesterol has no role in inhibiting NaBmediated iNOS [4]. Also, in an article by Brahmachari et al. [4], they measured the effects of cinnamon on mice with MS in which NaB reduced NF-κB activation and iNOS expression in glial cells by reducing p21ras activation, according to which oral administration of cinnamon powder [5] and drinking water containing NaB metabolite [4] suppresses iNOS and IL-1β expression in vivo in the spinal cord and cerebellum of EAE mice, these findings suggest that cinnamon is able to reduce in vivo inflammation in rat CNS EAE is also another feature of neurodegenerative disorders such as Alzheimer’s disease (AD) and Parkinson’s disease (PD), cinnamon and NaB. It also improves hippocampal function in an animal model of AD [6] and from nigrostriatum. Animal model PD Protects [7].
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