Atractylenolide I通过NF-κB通路减轻脑缺血再灌注损伤的作用研究

Abstract

Atractylenolide I is one of the main sesquiterpene lactones of Atractylodes macrocephala Koidz., Asteraceae, and its biological functions involved in cerebral ischemia/reperfusion damage were investigated by induction of middle cerebral artery occlusion in C57BL/6 mice for 2 h followed by reperfusion. Then, the effects of atractylenolide I were determined through assessment of infarct volume and brain water content. To mimic ischemia/reperfusion-like conditions in vitro , BV2 cells were exposed to oxygen–glucose deprivation/reoxygenation. Subsequently, cells were subjected to 0.01–1 μM atractylenolide I treatment. Cell viability and apoptosis were measured by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide assays and flow cytometry. Reverse-transcription quantitative polymerase chain reaction assays and western blotting were performed to measure the mRNA and protein levels. Lactase dehydrogenase release assay was conducted to determine cell damage. Inflammatory responses were identified by measuring the levels of pro-inflammatory mediators. Atractylenolide I alleviated the oxygen-glucose deprivation/reoxygenation–stimulated cell damage by decreasing cell apoptosis. Atractylenolide I reduced the levels of total triacylglyceride and total cholesterol in BV2 cells. Also, this bioactive sesquiterpene lactone ameliorated the oxygen-glucose deprivation/reoxygenation–induced inflammatory responses. In conclusion, atractylenolide I alleviates cerebral ischemia/reperfusion injury by reducing apoptosis and inflammatory responses through inactivation of the nuclear factor-κB pathway. Graphical Abstract