Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 31,822 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective 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.
Monday, April 21, 2025
Artemisinin alleviates ischemic stroke injury and promotes neurogenesis through PPARγ-mediated M2 polarization of microglia
Didn't your competent? stroke medical 'professionals' figure something useful with this years ago?
Ischemic
stroke (IS) remains a challenge in clinical treatment due to limited
therapeutic options. While artemisinin (ART), an antimalarial drug,
shields against acute IS via anti-inflammatory, antioxidant, and
anti-apoptotic properties, the long-term benefits and specific
underlying mechanisms have not been fully elucidated. Here, we
investigate whether ART ameliorates IS injury and promotes neurogenesis
by activating the peroxisome proliferator-activated receptor γ
(PPARγ)-dependent M2 microglial polarization.
Methods
The
experimental models included transient middle cerebral artery
occlusion/reperfusion (MCAO/R) in rats and oxygen-glucose
deprivation/reoxygenation (OGD/R) in primary microglial cultures to
simulate IS. The therapeutic effects of ART were evaluated by
neurological functions and infarct volume. PPARγ inhibitor T0070907
(T007) intraperitoneally injected 24 h following MCAO/R at a dose of 2
mg/kg in vivo and a concentration of 10 μM for 30 min before OGD in
vitro. We utilized real-time quantitative polymerase chain reaction
(RT-qPCR) along with Western blot analyses to detect the microglia
markers and PPARγ. The proliferation and differentiation of neural stem
cells (NSCs) both in vivo and in vitro were assessed via
immunofluorescence labeling. Neurogenic potential of ART-treated
microglia was investigated by conditioned medium. The levels of
brain-derived growth factor (BDNF) and insulin-like growth factor-1
(IGF-1) in microglia were measured by immunofluorescence staining and
enzyme-linked immunosorbent assay (ELISA).
Results
ART
treatment significantly alleviated short- and long-term neurological
deficits and reduced cerebral infarct volume in rats with IS.
Experiments conducted both in vivo and in vitro experiments illustrated
that ART directed microglia away from the pro-inflammatory M1 state
towards the anti-inflammatory M2 state, enhanced neurogenesis, and
upregulated the expression of PPARγ, BDNF, and IGF-1. In addition, the
conditioned medium from ART-exposed microglia stimulated the
proliferation and neuronal differentiation of primary NSCs. However,
these positive effects were effectively counteracted by the use of PPARγ
inhibitor T0070907 (T007).
Conclusion
Our
findings demonstrate that ART ameliorates IS injury and promotes
neurogenesis mainly through PPARγ-mediated microglia M2 polarization.
Therefore, ART can be considered a potential therapeutic drug for IS.
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