Open Access

Neuroprotective effects of galectin‑1 on cerebral ischemia/reperfusion injury by regulating oxidative stress

  • Authors:
    • Jie Zhao
    • Rui Zhu
    • Feifei He
    • Miao Wu
    • Yufu Wu
    • Xiangjun Meng
    • Xiaohong Liu
  • View Affiliations

  • Published online on: February 20, 2024     https://doi.org/10.3892/etm.2024.12442
  • Article Number: 154
  • Copyright: © Zhao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Oxidative stress contributes to the pathology of cerebral ischemia/reperfusion (I/R) injury. Galectin‑1 has shown an anti‑oxidative stress effect. The present study investigated whether this anti‑oxidative stress effect can account for the neuroprotective actions of galectin‑1 induced by cerebral I/R injury. A cerebral I/R injury model was created in C57Bl/6 mice by transient occlusion of the middle cerebral artery, after which the mice were treated with galectin‑1 for 3 days. Infarct volumes were measured. A rotarod test and neurological deficit score assessment was performed to evaluate the neurological deficits. Oxidative stress was evaluated by measuring the levels of reactive oxygen species (ROS) and lipid peroxidation malondialdehyde (MDA), while the anti‑oxidative stress status was assessed by measuring molecules such as catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidation enzyme (GSH‑Px) in the ischemic cerebral hemisphere of mice. The inflammatory cytokines, including Interleukin 1 (IL‑1), IL‑6 and tumor necrosis factor alpha (TNF‑α) were measured, and the expression of microglia was evaluated by immunohistochemistry in the ischemic cerebral hemisphere of mice. Galectin‑1 treatment ameliorated neurological deficits and reduced infarct volumes in the mice model with cerebral I/R injury. Moreover, it was demonstrated that galectin‑1 can significantly alleviate cerebral I/R injury in the ischemic cerebral hemisphere by decreasing the production of ROS and MDA, but increasing the production of CAT, SOD and GSH‑Px. Galectin‑1 treatment decreased microglia expression, and IL‑1, IL‑6 and TNF‑α levels in the ischemic cerebral hemisphere of mice. Galectin‑1 could improve the outcome of cerebral I/R injury by alleviating oxidative stress. Moreover, the neuroprotective effect of galectin‑1 in cerebral ischemia could be related to its anti‑oxidative stress effect.
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April-2024
Volume 27 Issue 4

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Spandidos Publications style
Zhao J, Zhu R, He F, Wu M, Wu Y, Meng X and Liu X: Neuroprotective effects of galectin‑1 on cerebral ischemia/reperfusion injury by regulating oxidative stress. Exp Ther Med 27: 154, 2024
APA
Zhao, J., Zhu, R., He, F., Wu, M., Wu, Y., Meng, X., & Liu, X. (2024). Neuroprotective effects of galectin‑1 on cerebral ischemia/reperfusion injury by regulating oxidative stress. Experimental and Therapeutic Medicine, 27, 154. https://doi.org/10.3892/etm.2024.12442
MLA
Zhao, J., Zhu, R., He, F., Wu, M., Wu, Y., Meng, X., Liu, X."Neuroprotective effects of galectin‑1 on cerebral ischemia/reperfusion injury by regulating oxidative stress". Experimental and Therapeutic Medicine 27.4 (2024): 154.
Chicago
Zhao, J., Zhu, R., He, F., Wu, M., Wu, Y., Meng, X., Liu, X."Neuroprotective effects of galectin‑1 on cerebral ischemia/reperfusion injury by regulating oxidative stress". Experimental and Therapeutic Medicine 27, no. 4 (2024): 154. https://doi.org/10.3892/etm.2024.12442