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 17, 2025

Buyang Huanwu decoction improves motor function by enhancing internal capsule reorganization through inhibiting Notch signaling after ischemic stroke

 The appeal to antiquity has no bearing on whether it works at all. We may as well go back to bloodletting as a stroke prescription as discussed in the 1843 book, 'An Essay On The Nature and Treatment of Apoplexy'.

Ask your doctor why they haven't gone back to bloodletting since they really haven't implemented any later research?

Buyang Huanwu decoction improves motor function by enhancing internal capsule reorganization through inhibiting Notch signaling after ischemic stroke

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https://doi.org/10.1016/j.jep.2025.119812
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Highlights

  • •
    BHD improves motor function in the ischemic stroke rats.
  • •
    BHD preserves structural integrity of the internal capsule after ischemic stroke.
  • •
    BHD-induced motor rehabilitation after stroke is related to internal capsule reorganization.
  • •
    BHD promotes the proliferation and differentiation of OPCs in the internal capsule.
  • •
    BHD inhibits Notch signal activation to benefit remyelination in the internal capsule.

Abstract

Ethnopharmacological relevance

Buyang Huanwu Decoction (BHD) is a common traditional Chinese medicine formula that has been used for the treating post-stroke disability for centuries. Nevertheless, the impact of BHD on internal capsule injury following stroke remains unknown and warrants further investigation.

Aim of the study

This study aimed to assess the efficacy of BHD on post-stroke internal capsule integrity by using an in vivo magnetic resonance imaging (MRI) technique and further explore the potential mechanisms by which BHD facilitates internal capsule reorganization after ischemic stroke.

Materials and methods

Male Sprague-Dawley rats were subjected to permanent occlusion of the middle cerebral artery (MCAO) to induce focal cerebral ischemia. BHD was intragastrically administered at doses of 16.6 g/kg and 8.3 g/kg to rats once daily for 30 consecutive days. Subsequently, an automated Digi gait system was utilized to assess the motor function. MRI examinations, including T2 relaxometry mapping and diffusion tensor imaging (DTI), were conducted to detect structural alterations in the internal capsule. Moreover, diffusion tractography was performed to evaluate internal capsule remodeling. Pearson correlation analysis was conducted between the gait and MRI parameters. Additionally, luxol fast blue (LFB) staining was performed for pathological assessment of the internal capsule. Double immunofluorescence staining was carried out to evaluate remyelination and Notch signaling activation in the injured internal capsule.

Results

The gait analysis revealed that BHD treatment significantly decreased stance time while elevating swing time, stride length, and paw area of the MCAO rats. T2 mapping indicated obvious infarction and an elevated T2 value, and DTI detected reduced fractional anisotropy but increased radial diffusivity in the internal capsule following MCAO. LFB staining further confirmed demyelination in the injured internal capsule. However, BHD interventions effectively reversed these MRI abnormalities and demyelination, and improved fiber density and length of the internal capsule. Notably, the gait performances were strongly correlated to the T2 value, fiber density, and fiber length of the internal capsule. Particularly, BHD treatments facilitated oligodendrogenesis in the internal capsule by elevating the numbers of Ki67/NG2, Ki67/Oligo2, and Ki67/CNPase positive cells. Furthermore, BHD effectively inhibited the activation of Notch signaling in the oligodendrocyte precursor cells (OPCs), as evidenced by reduced numbers of NG2/Notch1, NG2/NICD, and NG2/Hes5 positive cells.

Conclusion

The present study demonstrated that BHD could promote post-stroke motor recovery by alleviating structural damage to the internal capsule and facilitating internal capsule reorganization. Notably, BHD treatment enhanced oligodendrogenesis and subsequent remyelination by inhibiting Notch signaling activation in the OPCs.
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