【摘要】 目的 探讨丹参酮对脂多糖（LPS）诱导的肺泡Ⅱ型上皮细胞损伤的影响及其可能作用机制。方法 采用LPS诱导的肺泡Ⅱ型上皮细胞建立急性肺损伤模型，随机分组：空白对照组、LPS组、LPS+丹参酮L组、LPS+丹参酮M组、LPS+丹参酮H组、LPS+si-NC组、LPS+si-DLX6-AS1组、LPS+丹参酮+pcDNA-DLX6-AS1组；MTT法、流式细胞术分别就检测细胞增殖及凋亡；ELISA法检测白细胞介素-6(IL-6)、白细胞介素-10(IL-10)、肿瘤坏死因子-α（TNF-α）的水平；qRT-PCR法检测DLX6-AS1的表达量。结果 与空白对照组比较，LPS组细胞增殖抑制率和细胞凋亡率升高（P <0.05）,IL-6、IL-10、TNF-α的水平升高（P <0.05）,DLX6-AS1的表达量升高（P <0.05）；与LPS组相比，LPS+丹参酮H组、LPS+丹参酮L组、LPS+丹参酮M组细胞增殖抑制率和细胞凋亡率降低（P <0.05）,IL-6、IL-10、TNF-α的水平降低（P <0.05）,DLX6-AS1的表达量降低（P <0.05），且呈剂量依赖性；与LPS组、LPS+si-NC组比较，LPS+si-DLX6-AS1组细胞增殖抑制率和细胞凋亡率降低（P <0.05）,IL-6、IL-10、TNF-α的水平降低（P <0.05）；与LPS+丹参酮组比较，LPS+丹参酮+pcDNA-DLX6-AS1组细胞增殖抑制率和细胞凋亡率升高（P <0.05）,IL-6、IL-10、TNF-α的水平升高（P <0.05）。结论 丹参酮可通过抑制DLX6-AS1的表达而促进细胞增殖及抑制细胞凋亡、炎症反应从而减轻LPS诱导的肺泡Ⅱ型上皮细胞损伤。更多还原

【Abstract】 Objective:To explore the effect of tanshinone on lipopolysaccharide(LPS)-induced alveolar typeⅡ epithelial cell damage and its possible mechanism. Methods:LPS-induced alveolar type Ⅱ epithelial cells were used to establish an acute lung injury model,and they were randomly divided into groups:con group,LPS group,LPS+tanshinone L group,LPS+tanshinone M group,LPS+tanshinone H group,LPS+si-NC group,LPS+siDLX6-AS1 group,LPS+tanshinone+pcDNA-DLX6-AS1 group. MTT method and flow cytometry respectively were used to detect cell proliferation and apoptosis. ELISA method was used to detect the levels of IL-6,IL-10,and TNF-α；qRT-PCR was used to detect the expression of DLX6-AS1. Results:Compared with the con group,the cell proliferation inhibition rate and apoptosis rate in the LPS group were increased(P < 0.05),the levels of IL-6,IL-10,and TNF-α were increased(P < 0.05),and the expression of DLX6-AS1 was increased(P < 0.05). Compared with the LPS group,the cell proliferation inhibition rate and apoptosis rate of the LPS+tanshinone H group,LPS+tanshinone L group and LPS+tanshinone M group were decreased(P < 0.05),and the levels of IL-6,IL-10,and TNF-α were decreased(P < 0.05),the expression of DLX6-AS1 was decreased(P < 0.05),and was dose-dependent. Compared with the LPS group and LPS+si-NC group,the cell proliferation inhibition rate and apoptosis rate of the LPS+si-DLX6-AS1 group were reduced(P<0.05),and the levels of IL-6,IL-10,and TNF-α were reduced(P < 0.05). Compared with the LPS+tanshinone group,the cell proliferation inhibition rate and apoptosis rate of the LPS+tanshinone+pcDNA-DLX6-AS1 group were increased(P < 0.05),and the levels of IL-6,IL-10,and TNF-α were increased(P < 0.05). Conclusion:Tanshinone can promote cell proliferation and inhibit cell apoptosis and inflammation by inhibiting the expression of DLX6-AS1,thereby reducing LPS-induced alveolar type Ⅱepithelial cell damage.更多还原