Cryptotanshinone Attenuates Oxygen-Glucose Deprivation/ Recovery-Induced Injury in an in vitro Model of Neurovascular Unit

Sounds like this is fixing several of the 5 causes of the neuronal cascade of death in the first week.

Maybe these? Ask your doctor when a protocol is coming and who is working on fixing 3 and 5.

1.  glutamate poisoning
2.  excitotoxicity 

4.  Inflammatory action leaking through the blood brain barrier.

The latest here: 

Cryptotanshinone Attenuates Oxygen-Glucose Deprivation/ Recovery-Induced Injury in an in vitro Model of Neurovascular Unit

Hongye Zhao^1,2, Tiezheng Zheng¹, Xiaohan Yang¹, Ming Fan³, Lingling Zhu³, Shuhong Liu³, Liying Wu³ and Changkai Sun^1,4*

• ¹Department of Physiology and Key Laboratory of Brain Diseases of Liaoning Province, School of Basic Medical Sciences, Dalian Medical University, Dalian, China
• ²Department of Physiology, School of Basic Medical Sciences, Qiqihar Medical University, Qiqihar, China
• ³Department of Brain Protection and Plasticity, Institute of Basic Medical Sciences, Academy of Military Medical Sciences, Beijing, China
• ⁴Department of Biomedical Engineering, Faculty of Electronic Information and Electrical Engineering & Research Center for the Control Engineering of Translational Precision Medicine, Dalian University of Technology, Dalian, China

Cryptotanshinone (CTs), an active component isolated from the root of Salvia miltiorrhiza (SM), has been shown to exert potent neuroprotective property. We here established an oxygen-glucose deprivation/recovery (OGD/R)-injured Neurovascular Unit (NVU) model in vitro to observe the neuroprotective effects of CTs on cerebral ischemia/reperfusion injury (CIRI), and explore the underlying mechanisms. CTs was observed to significantly inhibit the OGD/R-induced neuronal apoptosis, and decease the activation of Caspase-3 and the degradation of poly-ADP-ribose polymerase (PARP), as well as the increase of Bax/Bcl-2 ratio in neurons under OGD/R condition. The inhibitory effects of CTs on neuron apoptosis were associated with the blocking of mitogen-activated protein kinase (MAPK) signaling pathway. CTs also remarkably ameliorated OGD/R-induced reduction of transepithelial electrical resistance (TEER) values and the increase of transendothelial permeability coefficient (Pe) of sodium fluorescein (SF) by upregulating the expression of ZO-1, Claudin-5, and Occludin in brain microvascular endothelial cells (BMECs), which might be related to the down-regulation of matrix metalloproteinase (MMP)-9 expression. Based on these findings, CTs may play a neuroprotective role in OGD/R injure in NVU models in vitro by inhibiting cell apoptosis and alleviating the damage of blood-brain barrier (BBB).