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目的研究黄芩苷对香烟烟雾提取物(cigarette smoke extract,CSE)诱导的人肺泡上皮细胞损伤的影响,并初步探讨其机制。方法制备CSE,用不同浓度黄芩苷对人肺泡上皮细胞A549进行预处理,再用CSE刺激细胞。用MTT法检测细胞存活率,流式细胞术测定细胞凋亡率,彗星实验观察DNA损伤情况,荧光法测定细胞内活性氧(reactive oxygen species,ROS)含量。结果随着CSE浓度的增加和作用时间的延长,细胞存活率下降,各组之间有统计学差异(P<0.05);黄芩苷能减少CSE诱导的细胞存活率下降,抑制CSE诱导的细胞内ROS的产生,并有剂量依赖关系(P<0.05或P<0.01);黄芩苷+CSE组细胞的彗星尾长、尾部DNA含量、尾距、Olive尾距均小于CSE组(P<0.05),并且黄芩苷可以减少CSE导致的细胞凋亡。结论黄芩苷可以拮抗CSE对细胞的损伤,提高细胞的存活率,降低凋亡率,其原因可能与黄芩苷能降低细胞ROS含量,减少DNA损伤有关。
Objective To study the effect of baicalin on the damage of human alveolar epithelial cells induced by cigarette smoke extract (CSE) and to explore its mechanism. Methods CSE was prepared by pretreatment of human alveolar epithelial cells A549 with baicalin at different concentrations, and then stimulated with CSE. The cell viability was measured by MTT assay, the apoptosis rate was measured by flow cytometry, the DNA damage was detected by comet assay, and the reactive oxygen species (ROS) content in cells was measured by fluorescence spectrometry. Results With the increase of CSE concentration and the prolongation of the action time, cell survival rate decreased, there was a statistical difference between the groups (P <0.05); Baicalin can reduce the cell survival rate induced by CSE, inhibition of CSE induced intracellular The production of ROS was dose-dependent (P<0.05 or P<0.01). The comet tail length, tail DNA content, tail distance, and Olive tail length of the baicalin+CSE group cells were smaller than those in the CSE group (P<0.05). And baicalin can reduce CSE-induced apoptosis. Conclusion Baicalin can antagonize the damage of CSE to cells, increase the survival rate of cells, and reduce the rate of apoptosis. The reason may be that baicalin can reduce ROS content and reduce DNA damage.