Open AccessAstragaloside and/or Hydroxysafflor Yellow A Attenuates Oxygen-Glucose Deprivation-Induced Cultured Brain Microvessel Endothelial Cell Death through Downregulation of PHLPP-1
Author(s) -
Jinyi Cao,
Kai Wang,
Lingeng Lu,
Lu Bai,
Ruimin Liang,
Yanjiang Qiao,
Jialin Duan,
Kai Gao,
Shanshan Cao,
Chunjiang Zhao,
Zhifu Yang
Publication year - 2020
Publication title -
evidence-based complementary and alternative medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.552
H-Index - 90
eISSN - 1741-4288
pISSN - 1741-427X
DOI - 10.1155/2020/3597527
Subject(s) - downregulation and upregulation , apoptosis , microvessel , pharmacology , in vitro , ischemia , medicine , stroke (engine) , programmed cell death , protein kinase b , reactive oxygen species , endothelial stem cell , reperfusion injury , biology , cancer research , microbiology and biotechnology , angiogenesis , biochemistry , mechanical engineering , gene , engineering
The incidence of ischemic stroke, a life-threatening condition in humans, amongst Asians is high and the prognosis is poor. In the absence of effective therapeutics, traditional Chinese medicines have been used that have shown promising results. It is crucial to identify traditional Chinese medicine formulas that protect the blood-brain barrier, which is damaged by an ischemic stroke. In this study, we aimed to elucidate such formulas. Brain microvascular endothelial cells (BMECs) were used to establish an in vitro ischemia-reperfusion model for oxygen-glucose deprivation (OGD) experiments to evaluate the function of two traditional Chinese medicines, namely, astragaloside (AS-IV) and hydroxysafflor yellow A (HSYA), in protecting against BMEC. Our results revealed that AS-IV and HSYA attenuated the cell loss caused by OGD by increasing cell proliferation and inhibiting cell apoptosis. In addition, these compounds promoted the migration and invasion of BMECs in vitro . Furthermore, we found that BMECs rescued by AS-IV and HSYA could be functionally activated in vitro , with AS-IV and HSYA showing synergetic effects in rescuing BMECs survival in vitro by reducing the expression of PHLPP-1 and activating Akt signaling. Our results elucidated the potential of AS-IV and HSYA in the prevention and treatment of stroke by protecting against cerebral ischemia-reperfusion injury.