Aims
In this study, we aimed investigate the impacts of CH-I on angiogenesis, effects for vascular structure changes and long-term neurological recovery after ischemic stroke as well as the potential mechanisms. Main
Methods
Young male mice subjected to intraluminal middle cerebral artery occlusion were administrated with CH-I once daily from day 1 to day 14 after stroke. The infarct volume was evaluated by TTC staining at day 7 after stroke. Neurological deficits were measured 1 to 28 days after stroke. Microvascular density, astrocyte coverage, and angiogenesis were assessed by IF, qRT-PCR, and WB at regular intervals after stroke. LSCI and TPMI measured changes in blood flow and vascular density and width from the day after stroke to day 28. Key findings: Compared with the dMCAO group, CH-I treatment significantly improved neurological recovery and reduced the infarct at day 7 after stroke. CH-I treatment increased the expression of the CD31, BrdU+/CD31+ microvessels and GFAP positive vessels in the peri-infarct cortex at day 7 to 28 after stroke. The expression of protein and gene were enhanced in CH-I group. CH-I significantly improved cerebral blood flow at day 7 after stroke. CH-I increased the vascular density and vascular width at day 14 after stroke. Significance: CH-I has been shown to restore nerve function, reduce the rate of cerebral infarction, increase microvascular density, and promote angiogenesis. CH-I improved cerebral blood flow, protected blood vessels from postoperative stenosis, and improved vascular plasticity.
Significance
CH-I has been shown to restore nerve function, reduce the rate of cerebral infarction, increase microvascular density, and promote angiogenesis. CH-I improved cerebral blood flow, protected blood vessels from postoperative stenosis, and improved vascular plasticity.