Electro-acupuncture-induced neuroprotection is associated with activation of the IGF-1/PI3K/Akt pathway following adjacent dorsal root ganglionectomies in rats

: 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.