Figure 5. MEG3 expression accelerated the process of IS by promoting Sema3A expression in vivo. (A) Expression level of MEG3 increased gradually at 4h, 8h, 24h point in the process of ischemia reperfusion (I/R stands for ischemic reperfusion). *P<0.05 vs sham. (B) Downregulation of MEG3 expression by si-MEG3 was proved significant. Simultaneous upregulation of Sema3A had little influence on the MEG3 expression. *P<0.05 vs control. (C) Sema3A expression was suppressed by si-MEG3, and the decrease was neutralized by manual Sema3A overexpression. *P<0.05 vs control, #P<0.05 vs si-MEG3. (D) Representative image of brain slices of three groups of rats. Normal tissues were a pink or red color, whereas the ischemic tissues were white. MCAO rats tend to have a bigger ischemic area in contrast with Sham group. Among MCAO rats, si-MEG3 group with MEG3 down-regulated have smaller ischemic area while it could be reversed by overexpression of Sema3A. (E) Quantified average percentage of the infarction area in the whole brain, the percentage was higher in MCAO rats compared with sham group. Among MCAO rats, the infarct volume decreased in si-MEG3 group, while simultaneous overexpression of Sema3A weakened the decrease. *P<0.05 vs sham, #P<0.05 vs MCAO, $P<0.05 vs MCAO+si-MEG3. (F) Neurological score rose in MCAO rats compared with sham rats. Among MCAO rats, si-MEG3 group had lower neurological score than MCAO control, while simultaneous overexpression of Sema3A neutralized the decrease of score. *P<0.05 vs sham, #P<0.05 vs MCAO, $P<0.05 vs MCAO+si-MEG3. (G) Expression of cleaved caspase-3, p-JNK and p-p38 increased significantly in MCAO group compared with control group. In si-MEG3 group, expression of cell apoptosis markers cleaved caspase-3 and phosphorylated levels of JNK and p38 decreased. Overexpression of Sema3A reversed the change. *P<0.05 vs sham, #P<0.05 vs MCAO, $P<0.05 vs MCAO+si-MEG3.