首页> 外文期刊>Molecular medicine reports >Electroacupuncture ameliorates learning and memory in rats with cerebral ischemia-reperfusion injury by inhibiting oxidative stress and promoting p-CREB expression in the hippocampus
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Electroacupuncture ameliorates learning and memory in rats with cerebral ischemia-reperfusion injury by inhibiting oxidative stress and promoting p-CREB expression in the hippocampus

机译:电针通过抑制氧化应激并促进海马中p-CREB的表达来改善脑缺血再灌注损伤大鼠的学习和记忆

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摘要

The present study aimed to investigate the mechanisms by which electroacupuncture (EA) ameliorates learning and memory in rats with cerebral ischemic-reperfusion (I/R) injury. Focal cerebral ischemia was induced in adult male Sprague-Dawley (SD) rats by transient middle cerebral artery occlusion (MCAO). Following MCAO surgery, the rats received EA at the Shenting (DU24) and Baihui (DU20) acupoints. The results of the present study demonstrated that treatment with EA significantly ameliorated neurological deficits and reduced cerebral infarct volume (P<0.05). In addition, EA improved the learning and memory ability of the rats, and markedly activated the cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB) signaling pathway, resulting in the inhibition of cerebral cell apoptosis in the ischemic penumbra. Furthermore, EA increased the activity of superoxide dismutase and glutathione peroxidase, the protein expression levels of phosphorylated-CREB and B-cell lymphoma 2 (Bcl-2), and the mRNA expression levels of Bcl-2. Conversely, EA decreased the levels of malondialdehyde and inhibited the expression levels of Bcl2-associated X protein. The results of the present study suggest that treatment with EA may result in the amelioration of learning and memory ability in rats with cerebral I/R injury.
机译:本研究旨在研究电针(EA)改善脑缺血再灌注(I / R)损伤大鼠的学习和记忆的机制。通过短暂性中脑动脉闭塞(MCAO)在成年雄性Sprague-Dawley(SD)大鼠中诱发局灶性脑缺血。 MCAO手术后,大鼠在神亭(DU24)和百会(DU20)穴位接受EA。本研究结果表明,电针治疗可明显改善神经功能缺损并减少脑梗死体积(P <0.05)。此外,EA改善了大鼠的学习和记忆能力,并显着激活了环状单磷酸腺苷(cAMP)反应元件结合蛋白(CREB)信号传导途径,从而抑制了缺血半影脑细胞的凋亡。此外,EA增加了超氧化物歧化酶和谷胱甘肽过氧化物酶的活性,磷酸化CREB和B细胞淋巴瘤2(Bcl-2)的蛋白质表达水平以及Bcl-2的mRNA表达水平。相反,EA降低了丙二醛的水平并抑制了Bcl2相关X蛋白的表达水平。本研究的结果表明,EA治疗可能会改善脑I / R损伤大鼠的学习和记忆能力。

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