PubMed article abstract display

Abstract

Background: Ischemic cerebrovascular disease (ICVD) is the third leading cause of death worldwide. Luteolin is a naturally flavonoid widely distributed in many plant leaves. This study aimed to explore the effects of luteolin on H₂O₂-induced ICVD cell oxidative injury model, as well as underlying molecular mechanisms.

Methods: Viability and apoptosis of PC-12 cells and rat brain microvascular endothelial cells (rBMECs) were detected using CCK-8 assay and FITC-Annexin V/PI staining, respectively. The levels of ROS and MDA were measured using DCFH-DA staining and MDA assay kit, respectively. Cell transfection was conducted to change the expression level of miR-21. Expression levels of key factors involved in cell proliferation, oxidative stress, apoptosis, PI3K/AKT and PDCD4/p21 pathways were evaluated using western blotting.

Results: Low concentration of luteolin had no significant effect on PC-12 cell viability and presented protective effects on H₂O₂-induced PC-12 cell viability loss, proliferation inhibition, ROS generation, oxidative stress increase and apoptosis. Moreover, luteolin up-regulated the expression level of miR-21 in H₂O₂-treated PC-12 cells. Overexpression of miR-21 strengthened the protective effects of luteolin on H₂O₂-induced PC-12 cell oxidative injury. Suppression of miR-21 had opposite effects. Furthermore, luteolin alleviated H₂O₂-induced inactivation of PI3K/AKT pathway and activation of PDCD4/p21 pathway in PC-12 cells by up-regulating miR-21. Besides, luteolin also protected rBMECs from H₂O₂-induced oxidative injury.

Conclusion: Our research revealed the protective effects of luteolin on H₂O₂-induced ICVD cell oxidative injury. Luteolin protected PC-12 cells from H₂O₂-induced oxidative injury by up-regulating miR-21, activating PI3K/AKT pathway and inactivating PDCD4/p21 pathway.

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