2. Academic Validation
  3. IL-11 ameliorates oxidative stress damage in neurons after spinal cord injury by activating the JAK/STAT signaling pathway

IL-11 ameliorates oxidative stress damage in neurons after spinal cord injury by activating the JAK/STAT signaling pathway

  • Int Immunopharmacol. 2023 Dec 30:127:111367. doi: 10.1016/j.intimp.2023.111367.
Yang Sun 1,  Xue Song 2,  Zhijun Geng 2,  Yibo Xu 3,  Linyu Xiao 4,  Yue Chen 4,  Bohan Li 3,  Jinran Shi 3,  Lian Wang 5,  Yueyue Wang 6,  Xiaofeng Zhang 2,  Lugen Zuo 5,  Jing Li 6,  Hezuo Lü 7,  Jianguo Hu 8
Affiliations

Affiliations

  • 1 Department of rehabilitation medicine, First Affiliated Hospital of Bengbu Medical University, Bengbu, Anhui, China.
  • 2 Department of Central Laboratory, First Affiliated Hospital of Bengbu Medical University, Bengbu, China; Inflammatory Bowel Disease Research Center, First Affiliated Hospital of Bengbu Medical University, Bengbu, China; Anhui Province Key Laboratory of Basic and Translational Research of Inflammation-related Diseases, Bengbu, China.
  • 3 Bengbu Medical University, Bengbu, China.
  • 4 Department of rehabilitation medicine, First Affiliated Hospital of Bengbu Medical University, Bengbu, Anhui, China; Bengbu Medical University, Bengbu, China.
  • 5 Inflammatory Bowel Disease Research Center, First Affiliated Hospital of Bengbu Medical University, Bengbu, China; Anhui Province Key Laboratory of Basic and Translational Research of Inflammation-related Diseases, Bengbu, China; Department of Gastrointestinal Surgery, First Affiliated Hospital of Bengbu Medical University, Bengbu, Anhui, China.
  • 6 Inflammatory Bowel Disease Research Center, First Affiliated Hospital of Bengbu Medical University, Bengbu, China; Anhui Province Key Laboratory of Basic and Translational Research of Inflammation-related Diseases, Bengbu, China; Department of Clinical Laboratory, First Affiliated Hospital of Bengbu Medical University, Bengbu, China.
  • 7 Anhui Province Key Laboratory of Basic and Translational Research of Inflammation-related Diseases, Bengbu, China; Department of Gastrointestinal Surgery, First Affiliated Hospital of Bengbu Medical University, Bengbu, Anhui, China. Electronic address: lhz233003@163.com.
  • 8 Inflammatory Bowel Disease Research Center, First Affiliated Hospital of Bengbu Medical University, Bengbu, China; Anhui Province Key Laboratory of Basic and Translational Research of Inflammation-related Diseases, Bengbu, China; Department of Clinical Laboratory, First Affiliated Hospital of Bengbu Medical University, Bengbu, China. Electronic address: jghu9200@163.com.
PMID: 38160564 DOI: 10.1016/j.intimp.2023.111367
Abstract

Objective: Excess Reactive Oxygen Species (ROS) generated by oxidative stress is a crucial factor affecting neuronal dysfunction after spinal cord injury (SCI). IL-11 has been reported to have antioxidative stress capacity. In the present study, we investigated the protective effect and mechanism of IL-11 against neuronal cell damage caused by oxidative imbalance.

Methods: We established a H2O2-induced oxidative stress injury model in PC12 cells and observed the effects of IL-11 on cellular activity, morphology, oxidase and antioxidant enzymes, and ROS release. Furthermore, the effect of IL-11 on Apoptosis of PC12 cells was assessed by flow cytometry, a TUNEL assay and Western blotting. Transcriptome analysis and rescue experiments revealed the mechanism by which IL-11 protects neurons from oxidative stress damage. For the in vivo investigation, an adenovirus-mediated IL-11 overexpression SCI rat model was constructed to validate the beneficial effect of IL-11 against SCI.

Results: IL-11 significantly improved the viability and enhanced the antioxidant activity of H2O2-treated PC12 cells while reducing ROS release. In addition, IL-11 reduced H2O2-induced PC12 cell Apoptosis. Transcriptome analysis revealed that the JAK/STAT pathway may be related to the antioxidant activity of IL-11. Treatment with a JAK/STAT Inhibitor (Stattic) exacerbated the oxidative damage induced by H2O2 and attenuated the protective effects of IL-11. The results of in vivo studies showed that IL-11 prevented neuronal Apoptosis due to oxidative imbalance and promoted the restoration of motor function in SCI rats by activating the JAK/STAT signaling pathway.

Conclusion: IL-11 inhibited oxidative stress-induced neuronal Apoptosis at least in part by activating the JAK/STAT signaling pathway and further promoted the recovery of motor function. These findings suggest that IL-11 may be an effective target for the treatment for SCI.

Keywords

Apoptosis; Interleukin 11; JAK/STAT; Neuron; Oxidative damage; Spinal cord injury.

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