The middle cerebral artery (MCA) is a common site of stroke in the human population. The middle cerebral artery occlusion (MCAO) model is widely recognized as the standard animal model for focal cerebral ischemia. The main procedure for inducing the MCAO model includes temporary occlusion of the common carotid artery (CCA), introduction of a suture into the internal carotid artery (ICA) or the transected external carotid artery (ECA), and tightening of the suture until blood supply to the MCA is interrupted.
Fig1. MCA occlusion model (MCAO) induced cerebrovascular diseases model.
Fig2.Pharmacological study of edaravone treatment in C57BL/6 MCAO model.
The collagenase-induced intracerebral hemorrhage (ICH) model is characterized by a simple induction procedure and a relatively high success rate. It effectively recapitulates the physiological and biochemical processes of spontaneous cerebral hemorrhage in human blood vessels, as well as the pathological progression of hematoma expansion following bleeding. To establish the model, animals are first anesthetized, disinfected, and fixed in a stereotaxic frame. A burr hole is drilled through the skull, and a microinjector needle is inserted into the caudate nucleus of one side of the rat brain under stereotaxic guidance. Different groups then receive an injection of 0.5 μL of collagenase into the caudate nucleus. Hemorrhage can be observed as early as 10 minutes after continuous observation, with pronounced symptoms that persist for an extended duration.
Fig1. Pharmacological study of edaravone treatment in collagenase-ICH C57BL/6 mouse model.
The bilateral carotid artery stenosis (BCAS) model is one of the commonly used models for studying cerebral small vessel disease. The construction method involves wrapping a microcoil with an inner diameter of 0.18 mm, a pitch of 0.50 mm, and a total length of 2.5 mm around the bifurcation of the common carotid artery on one side of the mouse. After a 30-minute interval, another microcoil is wrapped around the symmetrical position of the contralateral common carotid artery. At 22 days post-surgery, the mice exhibit significant short-term memory deficits. At 1 month post-surgery, pathological examination reveals white matter lesions in the corpus callosum, caudate putamen, internal capsule, and optic tract. At 6 months post-surgery, magnetic resonance imaging (MRI) detection shows severe white matter lesions, brain atrophy, and multiple focal subcortical infarcts.
Fig1. Bilateral carotid artery stenosis model of cerebrovascular diseases.
