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

xlomafota13 shared this article with you from Inoreader Insulin-like growth factor 1 promotes neurological functional recovery after spinal cord injury through inhibition of autophagy via the PI3K/Akt/mTOR signaling pathway Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1265. doi: 10.3892/etm.2021.10700. Epub 2021 Sep 6. 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 pathw ay. 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. Furthermor e, 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. PMID:34594402 | PMC:PMC8456500 | DOI:10.3892/etm.2021.10700 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.