title: [The effect of baicalin on human brain microvascular endothelial cell under the glucose deprivation combined with hypoxia condition].
abstract: OBJECTIVE
  To investigate the mechanisms of baicalin on anti-cerebral ischemic through observing the effect of baicalin on human brain microvascular endothelial cell under the glucose deprivation combined with hypoxia condition.
  
  
  METHODS
  Human brain microvascular endothelial cells (HBMVECs) cultured in vitro were divided into the following groups: normal group, model group, baicalin high dose group, baicalin middle dose group, baicalin low dose group, nimodipine group. The kits were used to detect the cell viability, leakage rate of lactate dehydrogenase (LDH), Na(+)-K(+)-ATPase, Ca(2+)-ATPase, the concentration of Ca2+ in each group, and apoptosis rates of each group were analyzed by flow cytometry (FCM).
  
  
  RESULTS
  Compared with the normal group, the cell viability, Na(+)-K(+)-ATPase and Ca(2+)-ATPase in model group decreased significantly (P < 0.01, P < 0.05). But the leakage rate of LDH, Ca2+ in cells and apoptosis rates increased remarkably (P < 0.01). Compared with the model group, the cell viability, Na(+)-K(+)-ATPase and Ca(2+)-ATPase increased obviously (P < 0.01, P < 0.05) in baicalin high dose group. But the leakage rate of LDH and Ca2+ in cells in baicalin high dose group decreased significantly comparing with that of model group (P < 0.05, P < 0.01). And the reduction of intracellular Ca2+ was superior to that of nimodipine group. Meanwhile, the apoptosis rates decreased significantly in both baicalin high and middle dose groups (P < 0.01).
  
  
  CONCLUSIONS
  Baicalin could improve the cell viability of HBMVECs under the glucose deprivation combined with hypoxia condition. And the mechanisms were related with improving the energy metabolism, inhibiting intracellular calcium overload and decreasing the apoptosis rate of cells further.
authors.affiliation: Affiliated Hospital of Chengde Medical College, Chengde 067000, China.
authors.forename: Hai-Bo
authors.initials: HB
authors.lastname: Xu
authors.affiliation: Affiliated Hospital of Chengde Medical College, Chengde 067000, China.
authors.forename: Zhi-Jun
authors.initials: ZJ
authors.lastname: Xing
authors.affiliation: Hebei Yiling Pharmaceutical Research Institute, Shijiazhuang 050035, China.
authors.forename: Zhi-Hong
authors.initials: ZH
authors.lastname: Li
authors.affiliation: Hebei Yiling Pharmaceutical Research Institute, Shijiazhuang 050035, China.
authors.forename: Zi-Qian
authors.initials: ZQ
authors.lastname: Zhang
authors.affiliation: Hebei Yiling Pharmaceutical Research Institute, Shijiazhuang 050035, China.
authors.forename: Jun-Qing
authors.initials: JQ
authors.lastname: Liang
authors.affiliation: Hebei Yiling Pharmaceutical Research Institute, Shijiazhuang 050035, China.
authors.forename: Zi-Ming
authors.initials: ZM
authors.lastname: Lv
mesh_terms: D017209:Apoptosis; D001921:Brain / Q000098:blood supply; D002118:Calcium / Q000378:metabolism; D002196:Capillaries / Q000166:cytology; D015687:Cell Hypoxia; D002470:Cell Survival; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000166:cytology* / Q000187:drug effects* / Q000378:metabolism; D005419:Flavonoids / Q000494:pharmacology*; D005947:Glucose / Q000737:chemistry; D006801:Humans
chemical_list: D005419:Flavonoids; C038044:baicalin; D005947:Glucose; D002118:Calcium