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.

中文翻译：

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绿茶多酚通过上调 lncRNA MALAT1 保护 PC12 细胞免受 H2O2 诱导的损伤。

减轻氧化损伤对于脊髓损伤（SCI）的治疗具有重要意义。研究已经确定绿茶多酚 (GTP) 对氧化损伤具有保护作用。在这项研究中，我们旨在研究 GTP 对 PC12 细胞中 H2O2 引起的损伤的保护作用，以及与长链非编码 RNA 转移相关的肺腺癌转录物 1 (MALAT1) 相关的分子基础。PC12 细胞在 H2O2 刺激之前用 GTP 预孵育。此外，MALAT1 缺陷 PC12 细胞是通过转染构建的，并通过定量实时聚合酶链反应 (qRT-PCR) 测定进行鉴定。接下来，分别通过细胞计数试剂盒-8 和流式细胞术检测细胞活力和细胞凋亡。同时，进行蛋白质印迹分析以监测与细胞凋亡相关的蛋白质（Bcl-2、Bax、pro-Caspase-3/9 和裂解的 Caspase-3/9）和自噬（微管相关蛋白 1 轻链 3 (LC3)-II、LC3-I、Beclin-1 和 p62)。此外，我们检查了 β-catenin 的表达并剖析了磷脂酰肌醇 3'-激酶 (PI3K) 和蛋白激酶 B (AKT) 的磷酸化。我们发现 H2O2 在启动细胞凋亡和自噬过程的同时降低了 PC12 细胞的活力。GTP预培养的PC12细胞保持活力并抵抗H2O2诱导的细胞凋亡和自噬。值得注意的是，GTP 预处理的 PC12 细胞在 H2O2 刺激后显示 MALAT1 增加。值得注意的是，GTP 的保护作用在 MALAT1 缺陷细胞中被缓冲，以响应 H2O2。β-catenin 的表达以及 PI3K 和 AKT 的磷酸化被 GTP 上调，而 MALAT1 敲低导致相反的结果。总之，GTP 通过 MALAT1 的上调保护 PC12 细胞免受 H2O2 诱导的损伤。这个过程可能是通过激活 Wnt/β-catenin 和 PI3K/AKT 信号通路。