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.

Saturday, June 28, 2025

Limonin attenuates neuroinflammation and enhances neurogenesis in a tMCAO mouse model of ischemic stroke

Do you really think your competent? doctor and hospital will ensure further human research gets done on this? I highly doubt it, but I could be surprised in 50 years when the research is finally done. 

Do you prefer your doctor and hospital incompetence NOT KNOWING? OR NOT DOING?

 Limonin attenuates neuroinflammation and enhances neurogenesis in a tMCAO mouse model of ischemic stroke


https://doi.org/10.21203/rs.3.rs-6879079/v1

This work is licensed under a CC BY 4.0 License

Neurogenesis in the subventricular zone (SVZ) is an effective way for brain repair after ischemic stroke. But neuroinflammation caused by cerebral ischemia would inhibit the effect of brain self-repair. As a Broadly active anti-inflammatory drugs, Limonin (LM) has a beneficial effect on ischemia-reperfusion(I/R) injury. However, the effect of LM on neurogenesis in the later stages of cerebral infarction is unknown. We speculate LM could generate anti-inflammation effect at the early stage of ischemic stroke and promote the subsequent neurogenesis. In our study, we used a transient middle cerebral artery occlusion (tMCAO) mouse model. We found LM treatment reduced the expression of iNOS and IL-1β proteins on day 3 after tMCAO. On day 7 after tMCAO, the number of BrdU/Nestin-positive cells around SVZ and BrdU/doublecortin (DCX)-positive cells in SVZ and the expression of Nestin, DCX proteins were increased through LM treatment. Moreover, on day 14 after tMCAO, the number of BrdU/DCX-positive cells in SVZ and peri-infarct area and the expression of DCX protein were increased in LM treated tMCAO mice. And LM treated tMCAO mice had fewer Cleaved-Caspase 3/DCX-positive cells in the peri-infarction zone compared to saline treated tMCAO mice 14 days after tMCAO. Finally, LM treatment increased the number of BrdU/NeuN-positive cells in the peri-infarct region and the expression of BDNF, GDNF, NGF proteins on day 14 after tMCAO. Our findings demonstrate that LM inhibits neuroinflammation and promotes neurogenesis after ischemic stroke.

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