Citation
- Authors: Vidyanti AN. et al.
- Year: 2020
- Journal: Inter J Mol Sci 21 2176
- Applications: in vivo / DNA / jetSI 10 mM
Method
Injection rate into each hippocampus: 0.4µl/minwith 26-gauge Hamilton syringe; DNA CRISPR-Cas (3 plasmid)
Abstract
The pathophysiology of vascular cognitive impairment (VCI) is associated with chronic cerebral hypoperfusion (CCH). Increased high-mobility group box protein 1 (HMGB1), a nonhistone protein involved in injury and inflammation, has been established in the acute phase of CCH. However, the role of HMGB1 in the chronic phase of CCH remains unclear. We developed a novel animal model of CCH with a modified bilateral common carotid artery occlusion (BCCAO) in C57BL/6 mice. Cerebral blood flow (CBF) reduction, the expression of HMGB1 and its proinflammatory cytokines (tumor necrosis factor-alpha [TNF-