南方医科大学学报

南方医科大学学报 ›› 2021, Vol. 41 ›› Issue (5): 729-735.doi: 10.12122/j.issn.1673-4254.2021.05.14

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木犀草素显著减轻镉诱导的肺上皮Beas-2B细胞的损伤

储 娜，张 璇，陈思远，甄 泉，王 允   

  • 出版日期:2021-05-20 发布日期:2021-06-11

Luteolin has a significant protective effect against cadmium-induced injury in lung epithelial Beas-2B cells

  • Online:2021-05-20 Published:2021-06-11

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摘要： 目的 研究木犀草素（LUT）对镉（Cd）诱导的人肺上皮Beas-2B细胞损伤的保护作用。方法 用不同浓度的木犀草素（0~160 μmol/L）或镉（0 ~40 μmol/L）处理Beas-2B细胞24 h，用MTT法检测细胞活性。用木犀草素（0.25、0.50和0.75 μmol/L）和/或 镉（5 μmol/L）处理Beas-2B细胞24 h，用MTT法检测细胞活性；用LD-L 微板法检测细胞乳酸脱氢酶（LDH）活性；用Hoechst荧光染色法观察细胞核形态变化；用DCFH-DA法测定细胞ROS水平；用WST-8法测定细胞SOD水平；用TBA法测定细胞GSH水平；用DTNB法测定细胞MDA水平，用Western blot检测细胞Akt、p-Akt和核因子E2相关因子2（Nrf2）蛋白的表达水平。结果 木犀草素在一定浓度范围内（0~80 μmol/L）不影响Beas-2B细胞的存活率（P>0.05），镉在5 μmol/L浓度水平时即可显著抑制Beas-2B细胞的生长（P<0.05），半数抑制浓度为24.6 μmol/L。木犀草素干预可不同程度地减轻镉处理引起的Beas-2B细胞活力的降低（P<0.05），减少镉处理组细胞LDH的释放量（P<0.05），改善镉处理组细胞的凋亡情况，抑制镉处理组细胞ROS水平的升高（P<0.05），增强镉处理组细胞SOD活性（P<0.05）和GSH含量（P<0.05），减少镉处理组细胞MDA的产生（P<0.05）。此外，木犀草素（0.5和0.75 μmol/L）干预可上调镉处理组细胞p-Akt和Nrf2的蛋白表达水平（P<0.05）。结论 木犀草素可显著减轻镉诱导的Beas-2B细胞的损伤，其机制可能与p-Akt和Nrf2蛋白表达水平的上调有关。

关键词: 木犀草素；镉；肺细胞；氧化应激

Abstract: Objective To investigate the protective effect of luteolin against cadmium (Cd)-induced injury in human lung epithelial Beas-2B cells. Methods Beas-2B cells were treated with different concentrations of luteolin (0-160 μmol/L) or Cd (0-40 μmol/L) for 24 h, and the cell viability was examined using MTT assay. After treatment with luteolin (0.25, 0.5 and 0.75 μmol/L) with or without Cd (5 μmol/L) for 24 h, the cells were examined for viability, lactate dehydrogenase (LDH) activity and morphological changes of the cell nuclei using Hoechst fluorescent staining. The levels of ROS, SOD, GSH and MDA in the treated cells were detected, and the expression levels of Akt, p-Akt and nuclear factor E2-related factor 2 (Nrf2) proteins were determined using Western blotting. Results Luteolin within the concentration range of 0- 80 μmol/L did not significantly affect the survival rate of Beas-2B cells (P>0.05), but Cd at 5 μmol/L significantly decreased the cell viability (P<0.05) with an IC50 of 24.6 μmol/L. In Cd-treated cells, treatment with luteolin significantly mitigated the decrease of cell viability, reduced LDH release and cell apoptosis, enhanced SOD activity and GSH content, and inhibited the production of MDA and ROS (all P<0.05). Luteolin also significantly up-regulated the expression levels of p-Akt and Nrf2 protein in Cd-treated Beas-2B cells (P<0.05). Conclusion Luteolin has a significant protective effect against Cd-induced injury in Beas-2B cells, and the effects are probably mediated, at least in part, by promoting the activation of Akt and Nrf2.

Key words: luteolin; cadmium; lung cells; oxidative stress