Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Thursday, April 25, 2019

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 Zhao1,2, Tiezheng Zheng1, Xiaohan Yang1, Ming Fan3, Lingling Zhu3, Shuhong Liu3, Liying Wu3 and Changkai Sun1,4*
  • 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).
Posted by at
Labels: , , , , , , , , ,

No comments:

Post a Comment

Subscribe to: Post Comments (Atom)