title: Effect of baicalin on oxygen-glucose deprivation-induced endothelial cell damage.
abstract: Baicalin, a plant-derived flavonoid, has been reported to exert neuroprotective effects on ischemia-like or excitotoxic injury. To confirm this function and explore the possible mechanism, we investigated the protective effect of baicalin on an in-vitro model of ischemia (oxygen-glucose deprivation-treated endothelial cell). In the present study, we found that baicalin (100 μM) inhibited cell death, reduced cell membrane damage, and maintained the integrity of the nucleus. Flow cytometric analysis and Hoechst 33258/propidium iodide double staining results showed that the necroptosis ratio decreased with baicalin treatment. Western blot analysis showed that baicalin regulated the expression of RIP-1 and RIP-3 in bEnd.3 cells and the use of detection kits showed that baicalin inhibited the production of reactive oxygen species and malondialdehyde, and increased the activity of superoxide dismutase in oxygen-glucose deprivation-treated bEnd.3 cells. These results indicated that baicalin effectively alleviated the oxidative stress, decreased the proportion of cells undergoing necrosis, and reduced cell damage.
authors.affiliation: aInstitute of Clinical Pharmacology bGuangzhou University of Chinese Medicine, Guangzhou, China.
authors.forename: Si
authors.initials: S
authors.lastname: Luo
authors.forename: Shi
authors.initials: S
authors.lastname: Li
authors.forename: Lei
authors.initials: L
authors.lastname: Zhu
authors.forename: Shu-Huan
authors.initials: SH
authors.lastname: Fang
authors.forename: Jun-Li
authors.initials: JL
authors.lastname: Chen
authors.forename: Qing-Qing
authors.initials: QQ
authors.lastname: Xu
authors.forename: Hong-Ying
authors.initials: HY
authors.lastname: Li
authors.forename: Na-Chuan
authors.initials: NC
authors.lastname: Luo
authors.forename: Cong
authors.initials: C
authors.lastname: Yang
authors.forename: Dan
authors.initials: D
authors.lastname: Luo
authors.forename: Lin
authors.initials: L
authors.lastname: Li
authors.forename: Xiao-Hui
authors.initials: XH
authors.lastname: Ma
authors.forename: Rong
authors.initials: R
authors.lastname: Zhang
authors.forename: Hong
authors.initials: H
authors.lastname: Wang
authors.forename: Yun-Bo
authors.initials: YB
authors.lastname: Chen
authors.forename: Qi
authors.initials: Q
authors.lastname: Wang
mesh_terms: D000818:Animals; D001921:Brain / Q000098:blood supply; D016923:Cell Death / Q000187:drug effects / Q000502:physiology; D015687:Cell Hypoxia / Q000187:drug effects* / Q000502:physiology; D002460:Cell Line; D002467:Cell Nucleus / Q000187:drug effects / Q000473:pathology / Q000502:physiology; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology; D042783:Endothelial Cells / Q000187:drug effects* / Q000473:pathology / Q000502:physiology; D005419:Flavonoids / Q000494:pharmacology*; D020690:GTPase-Activating Proteins / Q000378:metabolism; D005947:Glucose / Q000172:deficiency*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D055806:Microvessels / Q000187:drug effects / Q000473:pathology / Q000502:physiology; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D020011:Protective Agents / Q000494:pharmacology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D053422:Receptor-Interacting Protein Serine-Threonine Kinases / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D005419:Flavonoids; D020690:GTPase-Activating Proteins; D020011:Protective Agents; C490620:Ralbp1 protein, mouse; D017382:Reactive Oxygen Species; C038044:baicalin; D008315:Malondialdehyde; D007770:L-Lactate Dehydrogenase; D013482:Superoxide Dismutase; D053422:Receptor-Interacting Protein Serine-Threonine Kinases; C485615:Ripk3 protein, mouse; D005947:Glucose