VCAM1 Drives Vascular Inflammation Leading to Continuous Cortical Neuronal Loss Following Chronic Cerebral Hypoperfusion.

BACKGROUND: Chronic cerebral hypoperfusion (CCH) is associated with neuronal loss and blood-brain barrier (BBB) impairment in vascular dementia (VaD). However, the relationship and the molecular mechanisms between BBB dysfunction and neuronal loss remain elusive. OBJECTIVE: We explored the reasons for neuron loss following CCH. METHODS: Using permanent bilateral common carotid artery occlusion (2VO) rat model, we observed the pathological changes of cortical neurons and BBB in the sham group as well as rats 3d, 7d, 14d and 28d post 2VO. In order to further explore the factors influencing neuron loss following CCH with regard to cortical blood vessels, we extracted cortical brain microvessels at five time points for transcriptome sequencing. Finally, integrin receptor a4ß1 (VLA-4) inhibitor was injected into the tail vein, and cortical neuron loss was detected again. RESULTS: We found that cortical neuron loss following CCH is a continuous process, but damage to the BBB is acute and transient. Results of cortical microvessel transcriptome analysis showed that biological processes related to vascular inflammation mainly occurred in the chronic phase. Meanwhile, cell adhesion molecules, cytokine-cytokine receptor interaction were significantly changed at this phase. Among them, the adhesion molecule VCAM1 plays an important role. Using VLA-4 inhibitor to block VCAM1-VLA-4 interaction, cortical neuron damage was ameliorated at 14d post 2VO. CONCLUSION: Injury of the BBB may not be the main reason for persistent loss of cortical neurons following CCH. The continuous inflammatory response within blood vessels maybe an important factor in the continuous loss of cortical neurons following CCH.

[Preparation and characterization of kaolinite-potassium dihydrogen phosphate intercalation composite].

Thepotassium dihydrogenphospiate (KDP) intercalated kaolinite (K-KDP) was prepared by a three-step reaction. Firstly, polar dimethyl sulphoxide (DMSO) was introduced into the layers of kaolinite by ultrasonic method and the product K-DMSO was obtained as precursor; secondly DMSO was replaced by potassium acetate (KAc) and the product K-KAc was gotten as intermediate; finally KAc was replaced by KDP. The intercalation ratio of the final product K-KDP reached 81.3%. The structure of products at differentreaction process was characterized by Fourier-transformed infrared spectroscopy (FTIR), X-ray diffraction (XRD) and scanning electron microscope (SEM) in detail. FTIR results showed the existence of P==O in the final product but moved from 1300 to 1201 cm(-1). XRD results documented that the interlayer spacing of kaolinite was enlarged during the whole intercalation reaction. SEM indicated that the agglomeration of kaolinite was destroyed and the particle size distribution became more uniform.