Secondary Cerebellar Cortex Injury in Albino Male Rats after MCAO: A Histological and Biochemical Study

Abstract

The present study focused on secondary injury following the middle cerebral artery (MCA) occlusion in rats not linked to the MCA’s feeding zone. This entity has been very rarely studied. Additionally, this study investigated the rates of expression of five fundamental angiogenic biomarkers called endoglin, vascular endothelial growth factors-A (VEGF-A), endothelin-1 (ET-1), 2granulocyte colony-stimulating factor (G-CSF), and angiopoietin-using the MCA occlusion (MCAO) model. The random allocation of twelve adult male albino rats was in two groups. As a sham control group, six rats were used. This group was subjected to a sham operation without MCAO. The MCAO group consisted of six rats that were subjected to MCAO operation. After three days, the rats were sacrificed. The cerebellar specimens were immediately processed for light microscopic examination. An angiogenic biomarkers multiplex assay from multiplex was used to assess endoglin levels, VEGF-A, ET-1, angiopoietin-2, and G-CSF in serum samples. Hematoxylin and eosin-stained sections showed that the cerebellar cortex of rats of the MCAO group was more affected than the sham control group. Furthermore, Nissl stain and immunohistochemical analysis revealed an apparent increase in the number of positive immunoreactive in the cerebellar cortex and an evident decrease in Nissl granules in Purkinje cells of the MCAO rats, in contrast to the control rats. In addition, there was a significant increase in angiogenic factors VEGF-A, ET-1, angiopoietin-2, and endoglin. Interestingly, there was an increase in the G-CSF but a non-significant in the MCAO rats compared to the control rats. Furthermore, there was a significant correlation between the angiopoietin-2 and ET-1, and between G-CSF and ET-1. VEGF-A also exhibited significant positive correlations with the G-CSF serum level parameter, Endoglin, and ET-1. Rats subjected to MCAO are a suitable model to study secondary injury away from MCA’s feeding zone. Additionally, valuable insights into the association and interaction between altered angiogenic factors and acute ischemic stroke induced by MCAO in rats.

Experience of Middle Cerebral Artery Occlusion with Monofilament Technique and Investigation of Ischemia-Reperfusion-Related Structural Changes in Brain Tissue

“…In a study evaluating the morphological changes of brain cells after stroke, it was summarized that there were structural changes in the stem and axons of neurons in the ischemic area, vacuolization occurred in their plasms, and their nuclear structures were disrupted. They also noted the disintegration of Nissl granules, acidophilic cytoplasm, and red neuron formations disrupting protein structure (8,20). As a result of H&E staining in our samples, degenerated Purkinje cells, darkly stained cytoplasm, and spaces between nuclei and granular layer cells were visualized (Figure 2-B2).…”

“…Studies show that the pathological outcomes of experimental MCA-ischemia in rats and stroke in humans are similar (8).…”

Preclinical Evidence of Paeoniflorin Effectiveness for the Management of Cerebral Ischemia/Reperfusion Injury: A Systematic Review and Meta-Analysis

“…In vivo stroke models are now predominantly mice and rats, which is understandable given the lower costs of procurement and maintenance, as well as the ease of monitoring and tissue processing (Sommer, 2017). The intraluminal suture middle cerebral artery occlusion (MCAO) model, which does not need craniectomy, is the most commonly used experimental model for ischemic stroke in rats (Alrafiah, 2021).…”

Regulatory Effect of Electroacupuncture on Hypothalamic Serotonin and its Receptor in Rats with Cerebral Ischemia

“…The hypothalamus, which is a higher subcortical nerve center, is both a neuroendocrine regulatory center and a higher regulatory center of visceral activity. Hypothalamic injury causes pathological changes in some neurons, such as central chromatolysis, acute necrosis of neurons formed by neuronal nuclei consolidation and cytosolic shrinkage and deformation, and possibly the disintegration of myelin sheaths and axons and swelling of astrocytes [ 2 ]. These pathological changes can seriously affect neurological function.…”

“…Previous studies have shown that the nerve injury caused by middle cerebral artery occlusion (MCAO) is not only limited to local infarction but can also cause secondary injury to distant regions, such as the hypothalamus, thalamus, substantia nigra, cerebellum, and spinal cord [ 1 , 2 ]. Studies have shown that transient middle cerebral artery occlusion (tMCAO) in rats can cause apoptosis and autophagy in cells in the hypothalamus.…”