miR-128b Promotes Cerebral Infarction by Regulating the Expressions of BCL-2 and CAPASE3.

Abstract

To investigate the effect of miR-128b on apoptosis and BCL-2 and CAPASE3 expression in a rat middle cerebral artery occlusion (MCAO) model. The MCAO model was established by the thread embolism method. miR-128b agomir and antagomir were injected into the ventricle of MCAO rats by stereotaxic intracerebral injection. Then the rats were divided into a sham group, model group, miR-128b agomir group, and miR-128b antagomir group. Zea Longa was used to score the modeling rats. The area of cerebral infarction was assessed by 2,3,5-triphenyltetrazolium chloride staining. Apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling assay. The miR-128b relative expression was detected by real-time polymerase chain reaction. The expressions of BCL-2 and CAPASE3 were detected by immunohistochemistry and Western blotting. The MCAO model was constructed successfully. The expressions of miR-128b in the MCAO groups were higher than that of the sham group (P < 0.05). Compared with the model group, the cerebral infarction area in the miR-128b agomir group was significantly bigger and that of the miR-128b antagomir group was smaller (P < 0.05). The number of apoptotic cells in the miR-128b agomir group was more and that of miR-128b antagomir group was less (P < 0.05 vs. model group). The BCL-2 expression reduced and CAPASE3 expression increased in the MCAO groups (P < 0.05 vs. sham group). Compared with the model group, the Bcl-2 expression decreased and Caspase 3 expression increased in the miR-128b agomir group, and those in the miR-128b antagomir group were opposite. miR-128b promoted cerebral infarction in MCAO rats by regulating Bcl-2 and Caspase 3 expression.