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Evaluation of the Effects of Lipoic Acid and Spirulina platensis on Manganese-Induced Neurotoxicity in a Rat Model

机译:评价硫辛酸和螺旋藻浆料对大鼠锰诱导锰诱导的神经毒性的影响

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The aim of this study is to explore the ameliorative effects of α-lipoic acid (ALA) and/or Spirulina platensis (SP) against manganese (Mn)-induced brain damage. Sixty-four rats were classified into eight equal group, group I served as negative controls, group II received normal saline as a vehicle, group III treated with ALA (50 mg/kg/day), group IV treated with SP (300 mg/kg/day), group V treated with manganese chloride (MnCl2) at dosage of 74 mg/kg/five times/week, along with rats in groups VI (MnCl2/ALA), group VII (MnCl2/SP) and group VIII (MnCl2/ALA/SP). All treatments were administrated through oral route for eight-week, after that, the brain Mn, oxidant/antioxidant stress and inflammatory biomarkers, as well as the histopathological and immunohistochemical changes of the brain tissues were examined. Our results revealed that MnCl2 induced an overwhelming neurotoxicity evident by the elevation of brain Mn, serum protein carbonyl, brain tumor necrosis factor-α with reduction in serum superoxide dismutase and brain interleukin-10. Histologically, Mn accumulation caused structural damage, intense brain caspase-3 immuno-expression and induction of heat shock protein-70. Administration of ALA and/or SP significantly decreased the brain levels of Mn, reduce the inflammatory response, re-established the cytotoxic changes and downregulated the caspase-3 immunoexpression of HSP-70. We can conclude that simultaneous ALA and/or SP administration elicited the most favorable protective effects against the Mn-induced neurotoxicity.
机译:本研究的目的是探讨α-硫辛酸(ALA)和/或螺旋藻(SP)对锰(MN)诱导的脑损伤的改善作用。将六十四只大鼠分为八个相等的组,载为阴性对照组,II族接受甘氨酸作为载体,用ALA(50mg / kg /天)处理的III组,用SP治疗,IV组(300mg / KG /天),v族氯化锰(MnCl2)在74mg / kg /五次/周的剂量下处理,以及VI(MnCl2 / Ala),VII组(MNCl2 / SP)和viII组( mncl2 / ala / sp)。检查所有治疗后,通过口腔途径持续8周,之后,检查脑Mn,氧化剂/抗氧化应激和炎症生物标志物以及脑组织的组织病理学和免疫组化改变。我们的研究结果显示,MNCl2通过脑Mn,血清蛋白质羰基,脑肿瘤坏死因子-α降低诱导脑Mn,血清蛋白羰基,脑肿瘤坏死因子-α的巨大神经毒性。组织学上,Mn积累引起的结构损伤,强烈的脑Caspase-3免疫表达和热休克蛋白-70的诱导。 ALA和/或SP的施用显着降低了Mn的脑水平,降低了炎症反应,重新建立了细胞毒性变化,并下调了HSP-70的Caspase-3免疫表达。我们可以得出结论,同时ALA和/或SP管理局引发了对MN诱导的神经毒性最有利的保护作用。

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