miR101 aggravates cell apoptosis in cerebral ischemic area by downregulating JAK2

Cerebral ischemia can cause irreversible damage to neurons. As a member of the mRNA family, the effect of miR101 on ell apoptosis in various of cancers. However, the function of miR101 exert in ischemic injury through the regulation of JAK2 is still remain unknown. In current research, SPF rats were randomly separated into 4 groups: Sham group, MACO group, miR101 agomir group, and miR101 antagomir group, which were injected 10μl miR101 agomir and miR101 antagomir respectively into brain ventricle at 2 hours after MACO model establishment. As results, the miR101 expression in MACO group was increased compared to the sham group. Also, after miR101 agomir was applied, the percentage of thrombosis volume was increased compared to the MACO group, while miR101 antagomir obviously decreased the percentage of thrombosis volume. mNSS was elevated after miR101 agomir was injected, indicating the exacerbation of nerve function damage. It is also observed that miR101 agomir aggravates cell apoptosis after MACO model establishment, while miR101 antagomir alleviate the cell apoptosis. Both the expression of JAK2 and p-JAK2 were decreased after the injection of miR101 agomir compare to MACO group, while miR101 antagomir obviously increased the expression of JAK2 and p-JAK2. In conclusion, the overexpression of miR101 would aggravate the cerebral ischemia and thus exacerbate the loss of the nerve function. Also, the overexpression of miR101 exacerbate the cell apoptosis in brain tissues by downregulating the expression of JAK2 and JAK2 phosphorylation.