Electroacupuncture (EA) is widely recognized as clinical treatment of spinal cord injury (SCI). The purpose of this study is to elucidate whether and how the PI3K/AKT/mTOR signaling pathway plays any role in EA treating SCI. Rats were randomly divided into four equal groups: Control Group, Sham-operation Group, Model Group, and EA Group, then further randomly divided into the following subgroups: 1-day (), 1-day rapamycin (), 14-day (), and 28-day (). A rat model of SCI was established by a modified Allen’s weight-drop method. In the EA Group, rats were stimulated on Dazhui (GV14) and Mingmen (GV4) for 20 min by sterilized stainless steel needles. In the EA Group, the Basso, Beattie, and Bresnahan locomotor rating scale showed obvious improved locomotor function, and hematoxylin-eosin staining and magnetic resonance imaging showed that the histological morphology change of injured spinal cord tissue was obviously alleviated. Also, blocking spinal mTOR by injection of rapamycin showed that mTOR existed in the injured spinal cord, and EA could significantly activate mTOR in SCI rats. And immunohistochemistry and western blot analysis on the PI3K/AKT/mTOR signaling pathway showed that levels of PI3K, AKT, mTOR, and p70S6K in the injured spinal cord tissue were greatly increased in the EA Group, while the levels of PTEN and caspase 3 were decreased. The present study suggests that EA could affect cell growth, apoptosis, and autophagy through the PI3K/AKT/mTOR signaling pathway.

中文翻译：

---

大椎（GV14）和名门（GV4）电针对脊髓损伤后大鼠PI3K / AKT / mTOR信号通路的调节作用。

电针（EA）被广泛认为是脊髓损伤（SCI）的临床治疗方法。这项研究的目的是阐明PI3K / AKT / mTOR信号通路在EA治疗SCI中是否以及如何发挥作用。将大鼠随机分为四个相等的组：对照组，假手术组，模型组和EA组，然后进一步随机分为以下亚组：1天（），雷帕霉素1天（）， 14天（）和28天（）。通过改进的艾伦减肥法建立了SCI大鼠模型。在EA组中，用消毒的不锈钢针在大椎（GV14）和明门（GV4）上刺激大鼠20分钟。在EA组中，Basso，Beattie和Bresnahan的运动能力评分量表显示运动功能明显改善，苏木精-伊红染色和磁共振成像显示受伤的脊髓组织的组织形态学变化明显减轻。此外，通过注射雷帕霉素阻断脊髓mTOR的结果表明，受损脊髓中存在mTOR，而EA可以显着激活SCI大鼠的mTOR。对PI3K / AKT / mTOR信号通路的免疫组织化学和免疫印迹分析表明，在EA组中，受损脊髓组织中PI3K，AKT，mTOR和p70S6K的水平大大增加，而PTEN和caspase 3的水平下降。本研究表明，EA可以通过PI3K / AKT / mTOR信号通路影响细胞生长，凋亡和自噬。