RESUMO
Objective To investigate the effect of long non-coding RNA (IncRNA) nuclear-enriched abundant transcript 1 (NEATl) on hypoxia-reoxygenation (H/R) glial astrocyte injury, and to explore whether the mechanism was related to the regulation of micro RNA (miR)-761. Methods Rat cortical astrocytes were cultured to construct a H/R injury model. Astrocytes were divided into control group, model group, model+ small interfering RNA negative control (si-NC) group, model+ si-NEATl group, model+ miR-NC group, model + miR-761 group, model + si-NEATl + anti-miR-NC group, model+si-NEATl+anti-miR-761 group. Expression of NEATl and miR-761 were detected by Real-time PCR. The experiment was repeated 3 times. The content of malonaldefryde (MDA), and the activity of superoxide dismutase (SOD) and catalase (CAT) were detected by kits. Dual luciferase reporter experiment and Real-time PCR were used to analyze the targeting relationship between NEATl and miR-761. The experiment was repeated 3 times. Results Compared with the control group, the cell apoptosis rate and MDA content of the model group increased significantly, SOD and CAT activities decreased significantly, NEATl expression increased significantly, and miR-761 expression decreased significantly (P< 0. 05). Compared with the model+si-NC group, the apoptosis rate and MDA content of the model+si-NEATl group reduced significantly, and SOD and CAT activities increased significantly (P < 0 . 0 5) . Compared with the model + miR-NC group, the apoptosis rate and MDA content of the model + miR-761 group reduced significantly, and SOD and CAT activities increased significantly (P < 0 . 0 5) . MiR-761 was the target gene of N E A T l, and NEATl negatively regulated miR-761 expression. Compared with the model+si-NEATl+anti-miR-NC group, the apoptosis rate and MDA content of the model+siNEAT1+anti-miR-761 group increased significantly, and SOD and CAT activities decreased significantly (P < 0 . 0 5) . Conclusion Interference with NEATl expression can protect astrocytes from H / R injury by up-regulating miR-761.