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 insulin­like growth factor 1 (IGF­1) in mediating neuroplasticity in rats subjected to partial dorsal root ganglionectomies following electro­acupuncture (EA) treatment. The rats underwent bilateral removal of the L1­L4 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)­IGF­1, HSV­small interfering (si) RNA­IGF­1 and the associated control vectors were injected into the L5 DRG of rats in the EA Model group. HSV­IGF­1 transfection enhanced EA­induced neuroplasticity, which manifested as partial recovery in locomotor function, remission hyperpathia, growth of DRG­derived spared fibers, increased expression of phosphorylated (p­) phosphatidylinositol 3­kinase (PI3K) and Akt, and increased pPI3K/PI3K and pAkt/Akt expression ratios. By contrast, HSV­siRNA­IGF­1 treatment attenuated these effects induced by HSV­IGF­1 transfection. The results additionally demonstrated that HSV­IGF­1 transfection augmented the outgrowth of neurites in cultured DRG neurons, and interference of the expression of IGF­1 retarded neurite outgrowth. Co­treatment with a PI3K inhibitor or Akt siRNA inhibited the aforementioned effects induced by the overexpression of IGF­1. In conclusion, the results of the present study demonstrated the crucial roles of IGF­1 in EA­induced neuroplasticity following adjacent dorsal root ganglionectomies in rats via the PI3K/Akt signaling pathway.