Study On The Relationship Between The Regulation Of MiRNA-101 Associated With Apoptosis Factor JAK2 In The Rat Models Of MCAO

Objective:Research the relationship between miRNA-101 and apoptosis related factors jak2 in rat MCAO model. To investigate the miRNA-101 play in the’ MCAO rat model of anti apoptosis.Methods:The suture method to establish the model of focal cerebral infarction, intracerebral stereotaxic injection method miR-101 agomir or miR-101 antagomir injected into the lateral ventricle, to regulate the expression of miR-101; By mNSS score of rats after 24 hours neurological function; using triphenyl tetrazolium chloride (triphenyl tetrazolium chloride, TTC) staining method to assess infarct size; Detecting expression of brain tissue p-JAK2 by IEMA staining; Real-time PCR to detect the expression of miR-101, jak2 mRNA; Western Blot to detect p-JAK2 further expression in the brain tissue; The number of apoptotic cells was detected by Tunel;Using SSPS20.0 software package to process data results.Results:Model successfully established 60 cases,15 cases in each group. mNSS score showed that the mNSS score of each cerebral ischemia group was higher than that of sham operation group, the miRNA-101agomir group was higher than that of the simple cerebral infarction group, the miR-101 antagomir group was lower than the simple cerebral infarction group, P<0.05, the difference was statistically significant; TTC staining showed:sham operation group without infarction, cerebral ischemia group appear different degree of infarction, infarct volume miRNA-101 agomir group was higher than that of pure cerebral infarction group, the miR-101 antagomir group less than pure cerebral infarction group, P< 0.05, the difference has statistical significance; miR-101 expression:the expression of miR-101 in each cerebral ischemia group was higher than that in sham operation group, the miRNA-101 agomir group was higher than that of the simple cerebral infarction group, the miR-101 antagomir group was lower than the cerebral infarction group, P<0.05, the difference was statistically significant; jak2mRNA expression:Cerebral ischemia groups compared with the sham group jak2mRNA express varying degrees of decline, the expression of jak2mRNA was down regulated in the miRNA-101 agomir group than in the simple cerebral infarction group, the expression of jak2mRNA was higher in the miR-101 antagomir group than that in the cerebral infarction group, P<0.05, the difference was statistically significant; Western blot detection of p-jak2 protein: Compared with sham operated group, the expression of p-jak2 in cerebral infarction group and miRNA-101 agomir group decreased compared with sham operation group, The expression of p-jak2 was higher in the miR-101 antagomir group than in the cerebral infarction group, miRNA agomir group than pure cerebral infarction group p-jak2 decreased expression, miR-101 antagomir than a simple expression of cerebral infarction group p-jak2 rise, P<0.05, the difference was statistically significant; P-jak2 protein was detected by enzyme labeled staining:compared with sham operated group, the expression of p-jak2 was decreased in different degrees. miRNA-101 agomir group compared with the pure cerebral infarction group p-jak2 down-regulation and miR-101 antagomir group compared with the pure cerebral infarction group p-jak2 expression increased, the difference ,P<0.05, the difference was statistically significant; Tunel detecting ischemic penumbra apoptosis:Sham group microscope no apoptotic cells, brain ischemia group appeared different degree of apoptosis and the number of apoptotic cells excited miRNA-101 agomir group was greater than that of pure cerebral infarction group, the miR-101 antagomir group less than pure cerebral infarction group, P<0.05, the difference is statistically significant.Conclusion:1. miR-101 can be expressed in brain tissue, and the expression is significantly increased in cerebral ischemic penumbra;2. Agomir miR-101 and antagomir miR-101 can regulate the expression of miR-101 in brain tissue;3. Jak2 may be the target protein, and there is a negative relationship between the two;4. Jak2 expression changes occurred in the ischemic penumbra, jak2 may be involved in the regulation of apoptosis during cerebral ischemia;5. miR-101 in the process of cerebral infarction in rats may be involved in the regulation of apoptosis through the regulation of jak2.