Abstract

How to prevent cerebral ischemia-reperfusion injury (CI/R) is critical for treating ischemic stroke. LncRNA SNHG11 can participate in several diseases by competing endogenous RNA (ceRNA), but its’ role in CI/R is unclear. Hypoxia/reoxygenation model (H/R group) cells were set and separated into control team; H/R team; H/R+SNHG11 team and H/R+si-SNHG11 team followed by analysis of LncRNA SNHG11 by real-time PCR, LncRNA SNHG11 subcellular distribution by FISH assay, MTT assay for cell proliferation, flow cytometry for apoptosis, ROS and LDH content and PTEN expression by Western blot. In H/R group, SNHG11 level significantly increased and cell proliferation significantly decreased, along with increased cell apoptosis, ROS activity, LDH content and PTEN expression in comparison of control group (P-value less than 0.05); The foregoing variation was promoted further by the H/R group after overexpression of SNHG11 (P-value below 0.05) and reversed after transfection of SNHG1 siRNA (P <0.05). LncRNA SNHG11 is mainly localized on the cell membrane. miR-16 is a SNHG11 targeted miRNA. Transfection of miR-16 mimics into PC12 cells in H/R group can significantly promote cell proliferation, inhibit apoptosis, reduce ROS activity, LDH content and PTEN expression versus the H/R group (P-value less than 0.05). SNHG11 level in H/R condition is increased and might target miR-16 to regulate PTEN expression and oxidative stress, leading to apoptosis and damage.

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