Green tea polyphenols protect PC12 cells against H(2)O(2)-induced damages by upregulating lncRNA MALAT1

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 H(2)O(2)-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 H(2)O(2) 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 H(2)O(2) 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 H(2)O(2). Pointedly, GTP-pretreated PC12 cells showed an increase in MALAT1 after H(2)O(2) stimulation. Of note, the protective effects of GTP were buffered in MALAT1-deficient cells in response to H(2)O(2). 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 H(2)O(2)-induced damages by the upregulation of MALAT1. This process might be through activating Wnt/β-catenin and PI3K/AKT signal pathways.