大黄素对肺炎链球菌感染的肺泡上皮细胞损伤的作用及其机制研究

doi:10.3969/j.issn.1671-7171.2022.07.013

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摘要【目的】探讨大黄素对肺炎链球菌感染的肺泡上皮细胞损伤的作用及其机制研究。【方法】肺泡上皮细胞A549随机分为对照组、模型组、20 μg/mL组、40 μg/mL组、80 μg/mL组、160 μg/mL组,对照组细胞常规培养,其余组细胞均经过肺炎链球菌感染,20 μg/mL组、40 μg/mL组、80 μg/mL组、160 μg/mL组细胞在感染后24 h分别加入不同浓度的大黄素(20 μg/mL、40 μg/mL、80 μg/mL、160 μg/mL)处理。噻唑蓝(MTT)检测各组A549细胞的增殖;流式细胞术检测凋亡率;酶联免疫吸附测定法(ELISA)检测白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)水平;蛋白质印迹法检测A549细胞中B细胞淋巴瘤/白血病-2(Bcl-2)、Bcl-2相关X蛋白(Bax)、活化的含半胱氨酸的天冬氨酸蛋白水解酶3(Cleaved Caspase-3)、β-连环蛋白(β-catenin)、细胞周期蛋白D1(Cyclin D1)蛋白水平。【结果】与对照组相比,肺炎链球菌感染的A549细胞增殖活性、Bcl-2、β-catenin、Cyclin D1蛋白水平降低(P<0.05),凋亡率及IL-6、TNF-α、Bax和Cleaved Caspase-3蛋白水平增加(P<0.05);不同浓度大黄素促进肺炎链球菌感染的A549细胞增殖(P<0.05),抑制其凋亡(P<0.05),降低IL-6、TNF-α水平(P<0.05),增加Bcl-2蛋白水平(P<0.05),下调Bax和Cleaved Caspase-3蛋白水平(P<0.05),提高β-catenin、Cyclin D1蛋白水平(P<0.05)。【结论】大黄素可能通过调节Wnt/β-catenin信号通路从而促进肺炎链球菌感染的肺泡上皮细胞增殖,抑制其凋亡。

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	孙建荣
	赵静
	刘文林

关键词 ：肺炎链球菌, 肺泡上皮细胞/微生物学, 黄素类/药理学

Abstract：【Objective】 To investigate the protective effect of emodin on alveolar epithelial cell injury induced by Streptococcus pneumoniae and its mechanism. 【Methods】A549 alveolar epithelial cells were randomly divided into control group, model group and 20 μg/mL group, 40 μg/mL group, 80 μg/mL group, 160 μg/mL group, the cells in the control group were cultured routinely, and the cells in the other groups were infected by Streptococcus pneumoniae; 20 μg/mL group, 40 μg/mL group, 80 μg/mL group, 160 μg/mL group cells were added with different concentrations of emodin (20 μg/mL,40 μg/mL,80 μg/mL,160 μg/mL). The proliferation of A549 cells was detected by MTT; The apoptosis rate was detected by flow cytometry; Level of interleukin-6 (IL-6) and tumor necrosis factor-α(TNF-α)was detected by enzyme linked immunosorbent assay (ELISA) ; In A549 cells, B cell lymphoma / leukemia-2 (Bcl-2), Bcl-2 associated X protein (Bax), cleaved caspase containing cysteine-3(Cleaved Caspase-3),β-catenin and the protein levels of Cyclin D1 were detected by Western blot. 【Results】 Compared with the control group,the protein levels of the proliferative activity, Bcl-2, β-catenin and cyclin D1 decreased (P<0.05); The levels of apoptosis rate, IL-6 and TNF-α, Bax and cleared Caspase-3 protein increased (P<0.05); Different concentrations of emodin could promote the proliferation of A549 cells infected by Streptococcus pneumoniae (P<0.05), inhibit its apoptosis (P<0.05), and reduce IL-6 and TNF-α level (P<0.05), increase Bcl-2 protein level (P<0.05), decrease Bax and Cleaved Caspase-3 protein level (P<0.05) and increase protein levels of β-catenin and cyclin D1 (P<0.05). 【Conclusion】 Emodin may regulate Wnt/β-catenin signaling pathway, promote the proliferation of alveolar epithelial cells infected by Streptococcus pneumoniae and inhibit their apoptosis.

Key words： Streptococcus pneumoniae Alveolar Epithelial Cells/MI Flavins/PD

收稿日期: 2021-12-06

中图分类号:

R563.111

通讯作者: *E-mail:52514223@qq.com

引用本文:

孙建荣, 赵静, 刘文林. 大黄素对肺炎链球菌感染的肺泡上皮细胞损伤的作用及其机制研究[J]. 医学临床研究, 2022, 39(7): 1006-1009.
SUN Jian-rong, ZHAO Jing, LIU Wen-lin. Protective Effect of Emodin on Alveolar Epithelial Cell Injury Induced by Streptococcus Pneumoniae and its Mechanism. JOURNAL OF CLINICAL RESEARCH, 2022, 39(7): 1006-1009.

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http://journal07.magtech.org.cn/yxlcyj/CN/10.3969/j.issn.1671-7171.2022.07.013 或 http://journal07.magtech.org.cn/yxlcyj/CN/Y2022/V39/I7/1006

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