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橙皮苷,一种柑橘类黄酮,对C57BL/J6小鼠模型中的实验性自身免疫性脑脊髓炎(EAE)具有改善作用。

Hesperidin, a Citrus Flavonoid, Has the Ameliorative Effects Against Experimental Autoimmune Encephalomyelitis (EAE) in a C57BL/J6 Mouse Model.

作者信息

Ciftci Osman, Ozcan Cemal, Kamisli Ozden, Cetin Aslı, Basak Nese, Aytac Bilal

机构信息

Department of Medical Pharmacology, Faculty of Medicine, University of Inonu, 44280, Malatya, Turkey,

出版信息

Neurochem Res. 2015 Jun;40(6):1111-20. doi: 10.1007/s11064-015-1571-8. Epub 2015 Apr 10.

Abstract

The aim of this study was determined the effects of Hesperidin (HP) on neuronal damage in brain tissue caused by Experimental allergic encephalomyelitis (EAE), an established model of multiple sclerosis in C57BL/J6 mice. To explore 40 mice were equally divided into four groups: (1) Control, (2) EAE, (3) HP, and (4) HP + EAE. 14 days after induction of EAE with MOG35-55 and pertussis toxin, the mice treated with HP at the doses of 50 mg/kg/day for 7 days subcutaneously. To our results HP treatment prevents the oxidative stress caused by EAE via a decrease in lipid peroxidations and increase in elements of the antioxidant defense systems in brain tissue. Also, EAE elevate the IL-17, express the pro-inflammatory cytokines, and caspase-3-like immunreactivity, show apoptosis, staining in EAE mice brain and increased the incidence of histopathological damage. However, immonohistochemical and histological changes were reversed with HP. Moreover, elevated TNF-α and IL-1β levels, a result of EAE, were decreased in serum and neurological deficits as clinical signs were reversed with HP treatment in EAE mice, given HP. In conclusion, HP treatment effectively prevents oxidative, immunological and histological damage in the brain caused by EAE. It was thought that the beneficial effects of HP are likely a result of its strong antioxidant and anti-inflammatory properties.

摘要

本研究的目的是确定橙皮苷(HP)对实验性变应性脑脊髓炎(EAE)所致脑组织神经元损伤的影响,EAE是C57BL/J6小鼠多发性硬化的既定模型。为进行探究,将40只小鼠平均分为四组:(1)对照组,(2)EAE组,(3)HP组,(4)HP + EAE组。在用MOG35-55和百日咳毒素诱导EAE 14天后,以50 mg/kg/天的剂量对小鼠进行皮下注射HP,持续7天。根据我们的结果,HP治疗可通过降低脂质过氧化作用和增加脑组织中抗氧化防御系统的成分来预防EAE引起的氧化应激。此外,EAE会升高IL-17水平,表达促炎细胞因子,并增加caspase-3样免疫反应性,导致EAE小鼠脑内出现凋亡和染色,并增加组织病理学损伤的发生率。然而,HP可逆转免疫组织化学和组织学变化。此外,EAE导致的血清中TNF-α和IL-1β水平升高以及神经功能缺损,在给予HP治疗的EAE小鼠中随着临床症状的逆转而降低。总之,HP治疗可有效预防EAE引起的脑内氧化、免疫和组织学损伤。据认为,HP的有益作用可能是其强大的抗氧化和抗炎特性的结果。

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