Luteolin protected PC-12 cells from HO-induced oxidative injury. - GreenMedInfo Summary
Luteolin protects PC-12 cells from HO-induced injury by up-regulation of microRNA-21.
Biomed Pharmacother. 2019 Apr ;112:108698. Epub 2019 Feb 22. PMID: 30802826
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 HO-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 HO-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 HO-treated PC-12 cells. Overexpression of miR-21 strengthened the protective effects of luteolin on HO-induced PC-12 cell oxidative injury. Suppression of miR-21 had opposite effects. Furthermore, luteolin alleviated HO-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 HO-induced oxidative injury.
CONCLUSION: Our research revealed the protective effects of luteolin on HO-induced ICVD cell oxidative injury. Luteolin protected PC-12 cells from HO-induced oxidative injury by up-regulating miR-21, activating PI3K/AKT pathway and inactivating PDCD4/p21 pathway.