Ginkgo biloba repair spinal cord ischemia reperfusion injury in rats by regulating Ferroptosis signaling pathway

Author:

Zhang Fengyi1,Zhang Ding1,Guan Xiaoqing1,Zong Yuan1,Wang Hang1,Guo Li1,Shen Zhubing1,Yin Fei1

Affiliation:

1. Jilin University

Abstract

Abstract Ferroptosis is a hot topic in recent years. As a new type of cell death, its main signs are iron overload and lipid peroxidation.Spinal cord ischemia reperfusion injury (SCIRI) is often accompanied by reactive oxygen-induced oxidative stress, and the spinal cord is rich in polyunsaturated fatty acids, so it is very easy to undergo lipid peroxidation under the attack of oxygen free radicals after ischemia reperfusion injury, and eventually lead to degeneration and necrosis of nerve cells.Therefore, inhibition of reactive oxygen species accumulation is essential to reduce nerve cell death after SCIRI.Our previous studies have shown that Ginkgo biloba (GB) can remove oxygen free radicals produced during ischemia reperfusion in the spinal cord of rats, but the specific mechanism of action is unclear.In this study, we first obtained the genes of the SCIRI group and model group through bioinformatics analysis, and then intersects the genes related to ferroptosis to verify the most specific genes.After subsequent experiments, we found that Ginkgo biloba extract (GBE) can significantly increase glutathione peroxidase 4 (GPX4),solute carrier family7 member11 (SLC7A11) and augmenter of liver regeneration (ALR), decrease the expression of 4-hydroxy-2-nonenal (4-HNE) and transferrin receptor 1 (TfR1), alleviating nerve injury after SCIRI in rats.

Publisher

Research Square Platform LLC

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3