Long non-coding RNA LOC366613 alleviates the cerebral ischemic injury via regulating the miR-532-5p/phosphatase and tensin homolog axis

Abstract

Cerebral infarction (CI) has become a leading cause of death in China. Long non-coding RNAs (lncRNAs) are intensively involved in the progression of CI. Here, we aimed to investigate the effects of lncRNA LOC366613 (LOC366613) on cerebral I/R injury, as well as its possible mechanism. Transient middle cerebral artery occlusion (MCAO) was used to establish a mouse model of cerebral I/R, and the PC12 cell line was used to establish an in vitro oxygen-glucose deprivation (OGD) injury model. The MTT assay was used to determine cell viability, and qRT-PCR was used to determine RNA levels. Western blotting was conducted to detect protein expression levels. The TUNEL assay and flow cytometry were used to measure cell apoptosis, and 2,3,5-triphenyltetrazolium chloride (TTC) was used to determine cerebral infarct volume. Finally, RNA pull-down and luciferase activity assays were used to examine interactions between miR-532-5p and LOC366613, as well as between miR-532-5p and phosphatase and tensin homolog (PTEN). LOC366613 was overexpressed in patients with cerebral I/R injury. In PC12 cells, knockdown of LOC366613 reduced the apoptosis rate and lactic acid dehydrogenase (LDH) expression, while increasing cell viability. Moreover, miR-532-5p was shown to be a target of LOC366613, as predicted. Downregulation of miR-532-5p reversed the effects of LOC366613 knockdown on PC12 cell apoptosis, LDH release, and cell viability. Finally, PTEN was verified as a target of miR-532-5p. LOC366613 participates in cerebral I/R injury by regulating the miR-532-5p/PTEN axis, potentially providing a new CI treatment target.

Dietary Supplementation with Nervonic Acid Ameliorates Cerebral Ischemia‐Reperfusion Injury by Modulating of Gut Microbiota Composition‐Fecal Metabolites Interaction

“…Cerebral infarction, characterized by the obstruction of blood flow in the central nervous system resulting in ischemia and hypoxia, stands as a significant contributor to global mortality and disability. [ 1 ] The incidence of cerebral infarction, along with associated fatalities and the overall burden imposed by this condition, exhibits an annual upward trend. [ 2 ] The causes of cerebral infarction are complex, encompassing blood clot formation and the inadequate provision of vital nutrients such as oxygen and glucose to brain tissues, [ 3 ] resulting in significant ischemic and hypoxic damage.…”