7-days of FREE Audio papers, translation & more with Prime
7-days of FREE Prime access
7-days of FREE Audio papers, translation & more with Prime
7-days of FREE Prime access
https://doi.org/10.3892/ijmm.2018.4035
Copy DOIPublication Date: Dec 18, 2018 | |
Citations: 5 | License type: cc-by-nc-nd |
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.
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.