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首页> 外文期刊>Saudi Journal of Biological Sciences >Neuroprotective effect of aspirin combined with ginkgolide injection on cerebral ischemic stroke rats and its effect on ERK12 signal pathway
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Neuroprotective effect of aspirin combined with ginkgolide injection on cerebral ischemic stroke rats and its effect on ERK12 signal pathway

机译:阿司匹林结合甘油苷液对脑缺血性卒中大鼠的神经保护作用及其对ERK12信号途径的影响

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The main aim of this study was to evaluate the neuroprotective effect of aspirin combined with ginkgolide injection on cerebral ischemic stroke model rats and its effect on extracellular regulated protein kinase 1/2 (REK1/2) signaling pathway, and to clarify the possible mechanism of aspirin combined with ginkgolide injection on neuroprotective mechanism. Experimental rats were randomly divided into sham group, model group, aspirin group, ginkgolide group and combination group (aspirin? ?ginkgolide injection) (n?=?20). The results revealed scores of neurological dysfunction and infarct volume in aspirin group, ginkgolide group and combination group rats were lower than those in model group ( P ?0.05). Score of neurological dysfunction and the volume of cerebral infarction in combination group rats were lower than those in aspirin group and ginkgolide group ( P ?0.05). Combination of aspirin and ginkgolide injection could better reduce brain water content, reduce apoptosis rate of cortical cells P ?0.05, reduce expression levels of caspase-3, Bax and p-REK1/2 proteins in ischemic brain tissue P ?0.05, and increase expression level of Bcl-2 protein than aspirin and ginkgolide injection alone P ?0.05). In conclusion, the synergistic neuroprotective effect of aspirin and ginkgolide injection on cerebral ischemic stroke rats is better than that of aspirin and ginkgolide injection alone. The mechanism of action may be that the two compounds can play a synergistic role and inhibit the activation of REK1/2 signaling pathway, thus inhibiting apoptosis of nerve cells and exerting neuroprotective effect.
机译:本研究的主要目的是评估阿司匹林联合脑缺血性卒中模型大鼠的神经保护作用及其对细胞外调节蛋白激酶1/2(REK1 / 2)信号通路的影响,并阐明了可能的机制阿司匹林联合GinkGoolide注射针对神经保护机制的。实验大鼠被随机分为假组,模型组,阿司匹林基团,甘油三醇基组和组合组(阿司匹林?β-β-β2)。结果显示了阿司匹林组中的神经功能障碍和梗塞体积的评分,甘油三醇基组和组合组大鼠低于模型组(P& 0.05)。神经功能障碍的评分和组合组大鼠中的脑梗死的体积低于阿司匹林基团和甘油三醇基组(P& 0.05)。阿司匹林和甘油糖苷注射的组合可以更好地降低脑含水量,降低皮质细胞的凋亡率P& 0.05,降低缺血性脑组织中Caspase-3,Bax和P-Rek1 / 2蛋白的表达水平。0.05并且仅增加Bcl-2蛋白的表达水平,而不是阿司匹林和甘油甘脂注射液P& 0.05)。总之,阿司匹林和甘油醇内酯对脑缺血性卒中大鼠的协同神经保护作用优于单独的阿司匹林和甘油醇注射液。作用机制可能是两种化合物可以发挥协同作用并抑制REK1 / 2信号通路的激活,从而抑制神经细胞的凋亡并施加神经保护作用。

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