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Changes of complement and oxidative stress parameters in patients with acute cerebral infarction (ACI) or cerebral hemorrhage (CH), and their clinical significance were explored. A total of 122 patients with ACI or CH admitted to the People's Hospital of Zhangqiu Area from August 2018 to September 2019 were collected. There were 59 ACI patients assigned into a cerebral infarction group (CIG) and further 63 CH patients in a cerebral hemorrhage group (CHG). Additionally, 53 healthy people in physical examination during the same period were enrolled as a control group (CG). Both the CIG and the CHG were treated with edaravone, Xueshuantong, brain protein hydrolysates, aspirin and statin-related drugs. The levels of complement C3, complement C4, superoxide dismutase (SOD), and total antioxidant capacity (TAC) were determined. Receiver operating characteristic (ROC) curves were employed to analyze the predictive value of C3, C4, SOD and TAG in ACI and CH, and logistic regression was used to analyze the risk factors of stroke. Both CIG and CHG showed higher C3 level, and lower C4, SOD and TAC levels than the CG. The NIHSS <4 group and the NIHSS ≥4 group showed higher hs-C3 level, and lower SOD and TAC levels than the CG (all P<0.05), and the NIHSS <4 group showed lower C3 level and lower SOD and TAC levels than the NIHSS ≥4 group (all P<0.05). Hypertension and hyperlipidemia were independent risk factors of stroke. The serum complement and oxidative stress parameters in patients with ACI or CH can be determined through routine examination, and the nerve function deficit could be assessed by determining the complement and oxidative stress parameters in clinical practice. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]