4.6 Article

Houshiheisan compound prescription protects neurovascular units after cerebral ischemia

Journal

NEURAL REGENERATION RESEARCH
Volume 9, Issue 7, Pages 741-748

Publisher

WOLTERS KLUWER MEDKNOW PUBLICATIONS
DOI: 10.4103/1673-5374.131580

Keywords

nerve regeneration; brain injury; cerebral ischemia; Houshiheisan; wind-dispelling drugs; deficiency-nourishing drugs; neurovascular units; amyloid precursor protein; beta-amyloid; neuronal nuclear antigen; NSFC grant; neural regeneration

Funding

  1. National Natural Science Foundation of China [30973782, 81373526]
  2. Natural Science Foundation of Beijing [7102014, 7122018]
  3. Beijing Municipal Higher Learning Institution Talent Teaching Plan Young and Middle-aged Talented People Training Project [PXM2011014226]

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Houshiheisan is composed of wind-dispelling (chrysanthemun flower, divaricate saposhnikovia root, Manchurian wild ginger, cassia twig, Szechwan lovage rhizome, and platycodon root) and deficiency-nourishing (ginseng, Chinese angelica, large-head atractylodes rhizome, Indian bread, and zingiber) drugs. In this study, we assumed these drugs have protective effects against cerebral ischemia, on neurovascular units. Houshiheisan was intragastrically administered in a rat model of focal cerebral ischemia. Hematoxylin-eosin staining, transmission electron microscopy, immunofluorescence staining, and western blot assays showed that Houshiheisan reduced pathological injury to the ischemic penumbra, protected neurovascular units, visibly up-regulated neuronal nuclear antigen expression, and down-regulated amyloid precursor protein and amyloid-beta 42 expression. Wind-dispelling and deficiency-nourishing drugs maintained NeuN expression to varying degrees, but did not affect amyloid precursor protein or amyloid-beta 42 expression in the ischemic penumbra. Our results suggest that the compound prescription Houshiheisan effectively suppresses abnormal amyloid precursor protein accumulation, reduces amyloid substance deposition, maintains stabilization of the internal environment of neurovascular units, and minimizes injury to neurovascular units in the ischemic penumbra.

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