上调长链非编码 RNA SNHG12 表达减轻过氧化氢诱导的神经细胞活性下降及 细胞凋亡和过度自噬.

BACKGROUND: After spinal cord injury, secondary injury is considered to be a major factor in its high morbidity rate. Inhibiting the pathological cascade of oxidative stress and apoptosis and delaying the disease process are the primary therapeutic direction for alleviating spinal cord injury. The long non-coding RNA SNHG12 is thought to be related to cellular redox homeostasis, and its function on regulating the oxidative damage in neurons caused by H2O2 overload remains unknown. OBJECTIVE: To investigate the function and mechanism of long non-coding RNA SNHG12 in H2O2-induced oxidative damage of HT22 cells. METHODS: (1) The HT22 cells were exposed to 100 μmol/L H2O2 for 6 hours to establish the cellular oxidative damage model. (2) The expression level of SNHG12 in HT22 cells was increased by transfection. The influences of SNHG12 expression on HT22 cell viability, apoptosis level, and autophagy were evaluated using CCK8 assay, Tryphenol blue staining, TUNEL staining, and western blot analysis. (3) Luciferase assay was used to verify the targeting relationship between SNHG12/miR-320a/SIRT5. (4) The upregulation of miR-320a and SIRT5 in HT22 cells was induced by transfection, respectively, and the regulation of miR-320a and SIRT5 in the protective role of SNHG12 was explored by reverse experiments. RESULTS AND CONCLUSION: SHNG12 overexpression could alleviate the decline in cell viability, apoptosis, and excessive autophagy caused by H2O2. Luciferase reporter assay confirmed the binding relationship among SHNG12/miR-320a/SIRT5. miR-320a overexpression could reverse the effects of elevated SNHG12 on the above aspects, whereas SIRT5 overexpression can reverse the effect of up-regulation of miR-320a on the above indicators. It is concluded that SNHG12 suppressed autophagy and apoptosis of HT22 cells and alleviated oxidative damage via regulating miR-320a /SIRT5 axis. [ABSTRACT FROM AUTHOR]