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    张莉, 何达, 席俊峰. PRMT6通过抑制PTEN/β-catenin通路减轻脂多糖诱导的肺支气管上皮细胞损伤[J]. 徐州医科大学学报, 2021, 41(10): 729-736. DOI: 10.3969/j.issn.2096-3882.2021.10.005
    引用本文: 张莉, 何达, 席俊峰. PRMT6通过抑制PTEN/β-catenin通路减轻脂多糖诱导的肺支气管上皮细胞损伤[J]. 徐州医科大学学报, 2021, 41(10): 729-736. DOI: 10.3969/j.issn.2096-3882.2021.10.005
    shu
    PRMT6 reduces lipopolysaccharide-induced lung bronchial epithelial cell injury by inhibiting the PTEN/-catenin pathway[J]. Journal of Xuzhou Medical University, 2021, 41(10): 729-736. DOI: 10.3969/j.issn.2096-3882.2021.10.005
    Citation: PRMT6 reduces lipopolysaccharide-induced lung bronchial epithelial cell injury by inhibiting the PTEN/-catenin pathway[J]. Journal of Xuzhou Medical University, 2021, 41(10): 729-736. DOI: 10.3969/j.issn.2096-3882.2021.10.005
    shu

    PRMT6通过抑制PTEN/β-catenin通路减轻脂多糖诱导的肺支气管上皮细胞损伤

    PRMT6 reduces lipopolysaccharide-induced lung bronchial epithelial cell injury by inhibiting the PTEN/-catenin pathway

      摘要
    • 摘要: 目的 探究PRMT6对脂多糖（LPS）诱导的肺支气管上皮细胞损伤的作用及其可能的作用机制。方法 体外培养人支气管上皮细胞系16HBE，qRT-PCR检测细胞PRMT6 mRNA表达；Western blot检测细胞PRMT6、PTEN、p-β-catenin和β-catenin蛋白表达；CCK-8检测细胞活力；流式细胞术检测细胞凋亡和ROS产生；试剂盒检测细胞培养上清液中IL-1β、IL-6、TNF-α和MDA含量、SOD和LDH活性。结果 LPS呈剂量依赖性抑制细胞中PRMT6 mRNA和蛋白表达。与空白对照组相比，LPS组细胞中PRMT6 mRNA和蛋白表达、p-β-catenin/β-catenin蛋白表达明显降低（P＜0.05），细胞活力、SOD活性明显降低（P＜0.05），PTEN蛋白表达、细胞凋亡率、ROS、MDA、IL-1β、IL-6和TNF-α含量、LDH活性明显升高（P＜0.05），；与LPS组相比，LPS+oe- NC组细胞各指标差异均无统计学意义（P＞0.05）；与LPS+oe- NC组相比，LPS+oe- PRMT6组细胞中PRMT6 mRNA和蛋白表达、p-β-catenin/β-catenin蛋白表达明显升高（P＜0.05），细胞活力、SOD活性明显升高（P＜0.05），PTEN蛋白表达、细胞凋亡率、ROS、MDA、IL-1β、IL-6和TNF-α含量、LDH活性明显降低（P＜0.05）；与LPS+oe-PRMT6组相比，LPS+oe- PRMT6+oe-PTEN组细胞中PRMT6表达差异无统计学意义（P＞0.05），p-β-catenin/β-catenin蛋白表达明显降低（P＜0.05），细胞活力、SOD活性明显降低（P＜0.05），PTEN蛋白表达、细胞凋亡率、ROS、MDA、IL-1β、IL-6和TNF-α含量、LDH活性明显升高（P＜0.05）。结论 PRMT6通过抑制PTEN/β-catenin通路改善LPS诱导的肺支气管上皮细胞损伤

       

      Abstract: ob＜x＞jective To explore the effect of PRMT6 on lipopolysaccharide (LPS)-induced lung bronchial epithelial cell injury and its possible mechanism. Methods Human bronchial epithelial cell line 16HBE was cultured in vitro, and PRMT6 mRNA ex＜x＞pression was detected by qRT-PCR; The ex＜x＞pression of PRMT6, PTEN, p-β-catenin and β-catenin protein were detected by Western blot; cell viability was detected by CCK-8; Cell apoptosis and ROS production was detected by flow cytometry; the kit was used to detect the contents of IL-1β, IL-6, TNF-α and MDA, SOD and LDH activities in the cell culture supernatant . Results LPS inhibited the ex＜x＞pression of PRMT6 mRNA and protein in cells in a dose-dependent manner. Compared with the blank control group, the ex＜x＞pression of PRMT6 mRNA and protein, the ex＜x＞pression of p-β-catenin/β-catenin protein in the cells of the LPS group were significantly reduced (P<0.05), cell viability and SOD activity were significantly reduced (P<0.05), the ex＜x＞pression of PTEN protein, apoptosis rate, the content of ROS, MDA, IL-1β, IL-6 and TNF-α, and LDH activity were significantly increased (P<0.05); Compared with the LPS group, there’s no statistically significant differences in cell indicators of the LPS+oe-NC group (P>0.05); compared with the LPS+oe-NC group, the ex＜x＞pression of PRMT6 mRNA and protein in the LPS+oe-PRMT6 group , the ex＜x＞pression of P-β-catenin/β-catenin protein were significantly increased (P＜0.05), cell viability and SOD activity were significantly increased (P＜0.05), the ex＜x＞pression of PTEN protein, cell apoptosis rate, the content of ROS, MDA, IL- 1β, IL-6 and TNF-α, and LDH activity were significantly reduced (P＜0.05); Compared with the LPS+oe-PRMT6 group, the ex＜x＞pression of PRMT6 in the cells of the LPS+oe-PRMT6+oe-PTEN group was not significantly different (P>0.05), and the ex＜x＞pression of p-β-catenin/β-catenin protein was significantly reduced (P ＜0.05), cell viability and SOD activity were significantly reduced (P＜0.05), the ex＜x＞pression of PTEN protein, cell apoptosis rate, the content of ROS, MDA, IL-1β, IL-6 and TNF-α, and LDH activity were significantly increased (P <0.05). Conclusion PRMT6 can improve lung bronchial epithelial cell injury induced by LPS by inhibiting the PTEN/β-catenin pathway

       

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