Lin Ruhui, Lin Yukun, Tao Jing, Chen Bin, Yu Kunqiang, Chen Jixiang, Li Xiaojie, Chen Li-Dian
College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.
TCM Rehabilitation Research Center of SATCM, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.
Mol Med Rep. 2015 Nov;12(5):6807-14. doi: 10.3892/mmr.2015.4321. Epub 2015 Sep 14.
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.
本研究旨在探究电针改善脑缺血再灌注(I/R)损伤大鼠学习记忆能力的机制。采用成年雄性Sprague-Dawley(SD)大鼠,通过短暂大脑中动脉闭塞(MCAO)诱导局灶性脑缺血。MCAO手术后,大鼠在神庭穴(督脉24)和百会穴(督脉20)接受电针治疗。本研究结果表明,电针治疗显著改善神经功能缺损并减小脑梗死体积(P<0.05)。此外,电针改善了大鼠的学习记忆能力,并显著激活环磷酸腺苷(cAMP)反应元件结合蛋白(CREB)信号通路,从而抑制缺血半暗带区的脑细胞凋亡。此外,电针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)的蛋白表达水平以及Bcl-2的mRNA表达水平。相反地,电针降低了丙二醛水平并抑制了Bcl-2相关X蛋白(Bax)的表达水平。本研究结果提示,电针治疗可能改善脑I/R损伤大鼠的学习记忆能力。