粒体自噬
基因敲除
帕金
缺血
品脱1
细胞凋亡
再灌注损伤
医学
药理学
内科学
化学
自噬
生物化学
帕金森病
疾病
作者
Toushen Hong,Yang Zhou,Peng Li,Xiaoshuai Wu,Yixin Li,Yumei Li,Yong Zhao
出处
期刊:Neuroscience
[Elsevier]
日期:2022-02-01
卷期号:482: 30-42
被引量:7
标识
DOI:10.1016/j.neuroscience.2021.11.043
摘要
Cerebral ischemia-reperfusion injury (IRI) is caused by reperfusion following ischemia. Mitophagy is closely related to cerebral IRI. Mitophagy disorder or excess may be harmful and lead to neuronal apoptosis. Peroxiredoxin 6 (PRDX6) is an antioxidant protein and plays an important role in ischemic stroke. However, the relationship between PRDX6 and mitophagy is not clear at present. In order to explore and solve this problem. We have established a middle cerebral artery occlusion (MCAO) model of cerebral ischemia-reperfusion in SD rats and knockdown PRDX6 and PINK1 with lentivirus. Knocking down PRDX6 led to further aggravation of cerebral IRI. Our research found that knockdown PRDX6 increased the expression of mitophagy-related and apoptosis-related proteins. Knocking down PINK1 relieved mitophagy and apoptosis caused by knocking down PRDX6. In conclusion, knockdown of PRDX6 could aggravate cerebral IRI by enhancing PINK1/PARKIN pathway mediated mitophagy, and this effect could increase neuronal apoptosis.
科研通智能强力驱动
Strongly Powered by AbleSci AI