Jin Ma1, Lei Bao1, Xiaohua Xia1, Qiupeng Feng1, Yan Zhou1, Yingxin Wang1, Zhen Cao2. 1. Department of Emergency Medicine, The First People's Hospital of Kunshan, Kunshan City, Jiangsu Province, China. 2. Department of Emergency Medicine, The First People's Hospital of Kunshan, Kunshan City, Jiangsu Province, China. Electronic address: caozhen256@163.com.
Abstract
OBJECTIVE: To investigate the effect of miR-128b on apoptosis and BCL-2 and CAPASE3 expression in a rat middle cerebral artery occlusion (MCAO) model. METHODS: 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. RESULTS: 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. CONCLUSIONS: miR-128b promoted cerebral infarction in MCAO rats by regulating Bcl-2 and Caspase 3 expression.
OBJECTIVE: To investigate the effect of miR-128b on apoptosis and BCL-2 and CAPASE3 expression in a ratmiddle cerebral artery occlusion (MCAO) model. METHODS: The MCAO model was established by the thread embolism method. miR-128b agomir and antagomir were injected into the ventricle of MCAOrats 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. RESULTS: 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. CONCLUSIONS:miR-128b promoted cerebral infarction in MCAOrats by regulating Bcl-2 and Caspase 3 expression.