Abstract
The aim of this study was to explore the effect of micro ribonucleic acid (miR)-210 on neuronal apoptosis in rats with cerebral infarction (CI) by regulating the vascular endothelial growth factor (VEGF)-Notch signaling pathway. A total of 30 clean healthy male Sprague-Dawley rats weighing 200-300 g were selected and randomly divided into Sham group (n=10), CI model group (CIM group, n=10), and CIM + miR-210 Mimic group (n=10). The protein expression levels of VEGF, Notch1, cleaved-Caspase3 (c-Caspase3), B-cell lymphoma-2 (Bcl-2), and tubulin were detected via Western blotting. The messenger RNA (mRNA) levels of VEGF and Notch1 were detected via quantitative Polymerase Chain Reaction (qPCR). Meanwhile, the expression levels of VEGF and Notch1 in tissues were determined using immunohistochemistry. Furthermore, the apoptosis of tissues was determined via Annexin V-FITC, propidium iodide (PI) double labeling, and flow cytometry. The levels of VEGF and Notch1 increased significantly in the CIM group when compared with those in the Sham group (p<0.01). However, their expressions decreased remarkably in CIM + miR-210 Mimic group when compared with CIM group (p<0.05). The mRNA expressions of VEGF and Notch1 were evidently upregulated in the CIM group when compared with the Sham group (p<0.01), whereas they were remarkably downregulated in the CIM + miR-210 Mimic group than CIM group (p<0.05). Immunohistochemistry results indicated that the expression levels of VEGF and Notch1 in tissues were consistent with Western blotting results. Besides, the protein expressions of c-Caspase3 and Bcl-2 were remarkably higher in the CIM group than Sham group (p<0.01). However, they were significantly lower in the CIM + miR-210 Mimic group than those in the CIM group (p<0.05). In addition, flow cytometry results demonstrated that the apoptosis level increased significantly in CIM group when compared with the Sham group (p<0.05), while it was remarkably inhibited in the CIM + miR-210 Mimic group (p<0.05). MiR-210 can reduce the protein expressions of VEGF and Notch1, inhibit the VEGF-Notch signaling pathway, decrease the expression of pro-apoptotic factor c-Caspase3 and increase the expression of anti-apoptotic factor Bcl-2, thereby suppressing cerebral neuronal apoptosis and preventing CI-induced neuronal apoptosis.
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