Abstract
It is of significance to alleviate oxidative damages for the treatment of spinal cord injury (SCI). Studies have ascertained that green tea polyphenols (GTPs) exert protective activities against oxidative damages. In this study, we aimed to investigate the protective effects of GTP against H2O2-caused injuries in PC12 cells as well as the molecular underpinnings associated with long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1). PC12 cells were preincubated with GTP prior to H2O2 stimulation. Furthermore, MALAT1-deficient PC12 cells were constructed by transfection and identified by quantitative real-time polymerase chain reaction (qRT-PCR) assay. Next, viability and apoptosis were detected by cell counting kit-8 and flow cytometry, respectively. Meanwhile, Western blot assay was carried out to monitor the expression alteration of proteins associated with apoptosis (Bcl-2, Bax, pro-Caspase-3/9, and cleaved Caspase-3/9) and autophagy (microtubule-associated protein 1 light chain 3 (LC3)-II, LC3-I, Beclin-1, and p62). Moreover, we examined the expression of β-catenin and dissected the phosphorylation of phosphatidylinositol 3'-kinase (PI3K) and protein kinase B (AKT). We found that H2O2 decreased the viability of PC12 cells while initiated apoptosis and autophagy processes. GTP-preincubated PC12 cells maintained the viability and resisted the apoptosis and autophagy induced by H2O2. Pointedly, GTP-pretreated PC12 cells showed an increase in MALAT1 after H2O2 stimulation. Of note, the protective effects of GTP were buffered in MALAT1-deficient cells in response to H2O2. The expression of β-catenin and phosphorylation of PI3K and AKT were upregulated by GTP, while MALAT1 knockdown led to opposite results. To sum up, GTP protected PC12 cells from H2O2-induced damages by the upregulation of MALAT1. This process might be through activating Wnt/β-catenin and PI3K/AKT signal pathways.