LncRNA SNHG1 inhibits neuronal apoptosis in cerebral infarction rats through PI3K/Akt signaling pathway.

OBJECTIVE: To investigate the effects of long non-coding ribonucleic acid (lncRNA) small nucleolar RNA host gene 1 (SNHG1) on the neuronal apoptosis in rats with cerebral infarction through the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway. MATERIALS AND METHODS: Male Sprague Dawley (SD) rats were divided into M group (model control group), N group (rat model of cerebral infarction) and R group (rat model of cerebral infarction plus lncRNA SNHG1) and then treated accordingly. 2,3,5-triphenyl tetrazolium chloride (TTC) staining was applied to detect the percentage of cerebral infarct volume and apoptosis of brain cells in the three groups of rats; hematoxylin and eosin (HE) staining was utilized to observe the pathological morphology of brain tissues, and Western blotting was performed to measure the protein levels of phosphorylated PI3K (p-PI3K) and p-Akt in the brain tissues. RESULTS: The degree of neurological deficit in the N group was much higher than that in the M group (p<0.05), and it was decreased markedly in the R group compared with that in the N group, with statistically significant differences (p<0.05). In comparison with that in the M group, the cell apoptosis was aggravated notably in the N group and alleviated remarkably in the R group, and the differences were statistically significant (p<0.05). In the N group, the cerebral infarct volume accounted for 33.67% of the whole brain volume, and mild cerebral infarction was detected in the R group, with a percentage of cerebral infarct volume of 20.15%. N group had a more prominent increase in the cerebral infarct volume than the R group (p<0.05). Compared with those in the M group, the pyknotic nuclei and neuron staining of brain tissues were increased significantly, and the neuronal cell injury was aggravated in the N group, while markedly reduced pyknotic nuclei and neuron staining (p<0.05), as well as mild neuronal cell injury (p<0.05), were detected in the R group. The levels of p-PI3K and p-Akt proteins in the brain tissues declined remarkably in the N group compared with those in the R group (p<0.05). CONCLUSIONS: The protective effect of lncRNA SNHG1 on the rats with cerebral infarction is correlated with the activation of the PI3K/Akt signaling pathway. [ABSTRACT FROM AUTHOR]