Open Access

Insulin‑like growth factor 1 promotes neurological functional recovery after spinal cord injury through inhibition of autophagy via the PI3K/Akt/mTOR signaling pathway

  • Authors:
    • Duo Zhang
    • Yuan Yuan
    • Jichao Zhu
    • Di Zhu
    • Chenxi Li
    • Wei Cui
    • Lei Wang
    • Song Ma
    • Shuo Duan
    • Baoge Liu
  • View Affiliations

  • Published online on: September 6, 2021     https://doi.org/10.3892/etm.2021.10700
  • Article Number: 1265
  • Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Spinal cord injury (SCI) is a serious trauma; however, the mechanisms underlying the role of insulin‑like growth factor 1 (IGF‑1) in autophagy following SCI remain to be elucidated. The present study aimed to investigate the therapeutic effect of IGF‑1 on SCI and to determine whether IGF‑1 regulates autophagy via the PI3K/Akt/mTOR signaling pathway. SH‑SY5Y neuroblastoma cells were assigned to the H2O2, IGF‑1 and control groups to investigate subsequent neuron injury in vitro. An MTT assay was performed to evaluate cell survival. In addition, Sprague‑Dawley rats were randomly assigned to SCI, SCI + IGF‑1 and sham groups, and Basso‑Beatlie‑Bresnahan scores were assessed to determine rat neurological function. Western blotting was used to analyze the autophagy level and the activation of the PI3K/Akt/mTOR signaling pathway. Cell survival was increased significantly in the IGF‑1 group compared with the control group in vitro (P<0.05). Furthermore, neurological function was improved in the SCI + IGF‑1 group compared with the control group in vivo (P<0.05). The western blotting results further demonstrated that LC3II/LC3I expression was increased in the IGF‑1 group compared with the sham group in vivo and compared with the control group in vitro (both P<0.05). In the SCI + IGF‑1 group, the expression levels of PI3K, phosphorylated (p)‑Akt and p‑mTOR were higher compared with those in the sham and SCI groups in vivo (P<0.05). Moreover, in the IGF‑1 group, the expression levels of p‑Akt and p‑mTOR were higher compared with the control and the H2O2 groups in vitro (P<0.05). Collectively, the results of the present study suggested that IGF‑1 promoted functional recovery in rats following SCI through neuroprotective effects. Furthermore, the underlying mechanism may involve activation of the PI3K/Akt/mTOR signaling pathway, followed by inhibition of autophagy. However, further investigation into the association between IGF‑1‑regulated autophagy and the activation of different subtypes of PI3K is required.
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November-2021
Volume 22 Issue 5

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Zhang D, Yuan Y, Zhu J, Zhu D, Li C, Cui W, Wang L, Ma S, Duan S, Liu B, Liu B, et al: Insulin‑like growth factor 1 promotes neurological functional recovery after spinal cord injury through inhibition of autophagy via the PI3K/Akt/mTOR signaling pathway. Exp Ther Med 22: 1265, 2021
APA
Zhang, D., Yuan, Y., Zhu, J., Zhu, D., Li, C., Cui, W. ... Liu, B. (2021). Insulin‑like growth factor 1 promotes neurological functional recovery after spinal cord injury through inhibition of autophagy via the PI3K/Akt/mTOR signaling pathway. Experimental and Therapeutic Medicine, 22, 1265. https://doi.org/10.3892/etm.2021.10700
MLA
Zhang, D., Yuan, Y., Zhu, J., Zhu, D., Li, C., Cui, W., Wang, L., Ma, S., Duan, S., Liu, B."Insulin‑like growth factor 1 promotes neurological functional recovery after spinal cord injury through inhibition of autophagy via the PI3K/Akt/mTOR signaling pathway". Experimental and Therapeutic Medicine 22.5 (2021): 1265.
Chicago
Zhang, D., Yuan, Y., Zhu, J., Zhu, D., Li, C., Cui, W., Wang, L., Ma, S., Duan, S., Liu, B."Insulin‑like growth factor 1 promotes neurological functional recovery after spinal cord injury through inhibition of autophagy via the PI3K/Akt/mTOR signaling pathway". Experimental and Therapeutic Medicine 22, no. 5 (2021): 1265. https://doi.org/10.3892/etm.2021.10700