Electro-acupuncture-induced neuroprotection is associated with activation of the IGF-1/PI3K/Akt pathway following adjacent dorsal root ganglionectomies in rats
Electro-acupuncture-induced neuroprotection is associated with activation of the IGF-1/PI3K/Akt pathway following adjacent dorsal root ganglionectomies in rats
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DOI：
10.3892/ijmm.2018.4035
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发表时间：
2018-12
影响因子：
5.4
通讯作者：
Tao Hu;Min-Nan Lu;Bo Chen;Jun Tong;Rui Mao;Shan Li;Pin Dai;Ya-Xin Tan;Yan-Bin Xiyang
中科院分区：
文献类型：
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作者：
Tao Hu;Min-Nan Lu;Bo Chen;Jun Tong;Rui Mao;Shan Li;Pin Dai;Ya-Xin Tan;Yan-Bin Xiyang
本研究旨在探讨胰岛素样生长因子-1(IGF-1)在电针治疗背根节部分切除大鼠神经可塑性中的作用及其机制。电针模型组大鼠切除双侧L1~L4和L6背根节，保留L5背根节，分别在足三里-旋中和福图-三阴交两对穴位进行28d的电针治疗。接受背根神经节部分切除而不经电针治疗的大鼠作为对照组(模型组)。随后将单纯疱疹病毒(HSV)-IGF-1、HSV-siRNA-IGF-1及相关对照载体注入电针模型组大鼠L5背根节。HSV-IGF-1基因转染可增强电针诱导的神经可塑性，表现为运动功能部分恢复，缓解过敏，DRG来源的备用纤维生长，磷酸化(p-)磷脂酰肌醇3-激酶(PI3K)和Akt表达增加，pPI3K/PI3K和Pakt/Akt表达增加。相反，HSV-siRNA-IGF-1处理可减弱HSV-IGF-1的这些效应。结果还表明，HSV-IGF-1基因可以促进培养的背根节神经元突起的生长，而干扰IGF-1的表达则抑制了突起的生长。与PI3K抑制剂或Akt siRNA共同处理可抑制IGF-1过表达所诱导的上述效应。综上所述，本研究结果表明，IGF-1通过PI3K/Akt信号通路在电针诱导的大鼠邻近背根神经节切除后的神经可塑性中发挥重要作用。
The aim of the present study was to investigate the putative role and underlying mechanisms of insulin-like growth factor 1 (IGF-1) in mediating neuroplasticity in rats subjected to partial dorsal root ganglionectomies following electro-acupuncture (EA) treatment. The rats underwent bilateral removal of the L1-L4 and L6 dorsal root ganglia (DRG), sparing the L5 DRG, and were subsequently subjected to 28 days of EA treatment at two paired acupoints, zusanli (ST 36)-xuanzhong (GB 39) and futu (ST 32)-sanyinjiao (SP 6), as the EA Model group. Rats that received partial dorsal root ganglionectomies without EA treatment served as a control (Model group). Subsequently, herpes simplex virus (HSV)-IGF-1, HSV-small interfering (si) RNA-IGF-1 and the associated control vectors were injected into the L5 DRG of rats in the EA Model group. HSV-IGF-1 transfection enhanced EA-induced neuroplasticity, which manifested as partial recovery in locomotor function, remission hyperpathia, growth of DRG-derived spared fibers, increased expression of phosphorylated (p-) phosphatidylinositol 3-kinase (PI3K) and Akt, and increased pPI3K/PI3K and pAkt/Akt expression ratios. By contrast, HSV-siRNA-IGF-1 treatment attenuated these effects induced by HSV-IGF-1 transfection. The results additionally demonstrated that HSV-IGF-1 transfection augmented the outgrowth of neurites in cultured DRG neurons, and interference of the expression of IGF-1 retarded neurite outgrowth. Co-treatment with a PI3K inhibitor or Akt siRNA inhibited the aforementioned effects induced by the overexpression of IGF-1. In conclusion, the results of the present study demonstrated the crucial roles of IGF-1 in EA-induced neuroplasticity following adjacent dorsal root ganglionectomies in rats via the PI3K/Akt signaling pathway.