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胡黄连苷Ⅱ对非小细胞肺癌恶性进展的影响
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| 篇名： | 胡黄连苷Ⅱ对非小细胞肺癌恶性进展的影响 |
| TITLE： | Effect of picroside Ⅱ on the malignant progression of non-small cell lung cancer |
| 摘要： | 目的 探讨胡黄连苷Ⅱ对非小细胞肺癌（NSCLC）恶性进展的影响及机制。方法将A549细胞分组为对照组，胡黄连苷Ⅱ低、中、高浓度组，K6PC-5[鞘氨醇激酶1（SPHK1）激活剂]组，胡黄连苷Ⅱ高剂量+K6PC-5组，检测细胞增殖、迁移、侵袭情况，以及细胞中增殖细胞核抗原（PCNA）、基质金属蛋白酶2（MMP-2）、MMP-9、SPHK1、1-磷酸鞘氨醇受体3（S1PR3）及胞外信号调节激酶1/2（ERK1/2）蛋白的表达情况。以BALB/c裸鼠为对象，通过皮下接种A549细胞悬液建立NSCLC裸鼠移植瘤模型，并将其分为裸鼠-对照组，裸鼠-胡黄连苷Ⅱ低、中、高剂量组，裸鼠-K6PC-5组，裸鼠-胡黄连苷Ⅱ高剂量+K6PC-5组（每组5只），考察胡黄连苷Ⅱ对其瘤体质量及体积的影响。结果与对照组比较，胡黄连苷Ⅱ低、中、高浓度组的细胞OD450值、EdU阳性细胞率、划痕愈合率、细胞侵袭数及PCNA、MMP-2、MMP-9、SPHK1、S1PR3、ERK1/2蛋白的相对表达量均显著降低；与裸鼠-对照组比较，裸鼠-胡黄连苷Ⅱ低、中、高剂量组裸鼠体内的瘤体质量及体积均显著降低或缩小，上述指标均呈浓度/剂量依赖性变化（P＜0.05）；K6PC-5组细胞和裸鼠-K6PC-5组裸鼠对应指标的变化趋势则相反（P＜0.05）。与胡黄连苷Ⅱ高浓度组或裸鼠-胡黄连苷Ⅱ高剂量组比较，胡黄连苷Ⅱ高浓度+K6PC-5组细胞和裸鼠-胡黄连苷Ⅱ高剂量+K6PC-5组裸鼠的上述定量指标均显著升高或增大（P＜0.05）。结论胡黄连苷Ⅱ可能通过抑制SPHK1/1-磷酸鞘氨醇/S1PR3信号通路来抑制NSCLC的恶性进展。 |
| ABSTRACT： | OBJECTIVE To investigate the effect and mechanism of picroside Ⅱ on the malignant progression of non-small cell lung cancer （NSCLC）. METHODS A549 cells were divided into the control group， picroside Ⅱ low-， medium- and high- concentration groups， K6PC-5 [sphingosine kinase 1 （SPHK1） activator] group， and picroside Ⅱ high-dose+K6PC-5 group. Cell proliferation， migration and invasion were detected. Besides， the expression of proliferating cell nuclear antigen （PCNA）， matrix metalloproteinase-2 （MMP-2）， MMP-9， SPHK1， sphingosine-1-phosphate receptor 3 （S1PR3） and extracellular signal-regulated kinase 1/2 （ERK1/2） protein in the cells were also observed. BALB/c nude mice were subcutaneously inoculated with A549 cell suspension to establish NSCLC xenograft models. Then they were assigned to the nude mouse-control group， nude mouse-picroside Ⅱ low-， medium- and high-dose groups， nude mouse-K6PC-5 group， and nude mouse-picroside Ⅱ high-dose+K6PC-5 group （with 5 mice in each group） to investigate the effect of picroside Ⅱ on their tumor mass and volume. RESULTS Compared with the control group， the OD450 values， EdU-positive cell rates， scratch healing rates， cell invasion number， and the relative expression levels of PCNA， MMP-2， MMP-9， SPHK1， S1PR3 and ERK1/2 protein in the low-， medium- and high-concentration groups of picroside Ⅱ were significantly decreased. Compared with the nude mouse-control group， the tumor mass and volume in the nude mouse-low-， medium- and high-dose groups of picroside Ⅱ were significantly decreased or shrunk. The changes of above indicators were concentration/dose-dependent （P＜0.05）. The changing trend of the corresponding indicators in the K6PC-5 ZYTS181） group and the nude mouse-K6PC-5 group was opposite （P＜0.05）. Compared with the picroside Ⅱ high-concentration group or the nude mice-picroside Ⅱ high-dose group， the above quantitative indicators in the picroside Ⅱ high- concentration+K6PC-5 group cells and the nude mouse-picroside Ⅱ high-dose+K6PC-5 group nude mice were significantly increased or enlarged （P＜0.05）. CONCLUSIONS Picroside Ⅱ may inhibit the malignant progression of NSCLC by inhibiting SPHK1/sphingosine-1-phosphate/S1PR3 signaling pathway. |
| 期刊： | 2024年第35卷第04期 |
| 作者： | 郭寰宇；王卫芳；徐丽伟；董文博 |
| AUTHORS： | GUO Huanyu，WANG Weifang，XU Liwei，DONG Wenbo |
| 关键字： | 胡黄连苷Ⅱ；非小细胞肺癌；增殖；迁移；侵袭；鞘氨醇激酶1/1-磷酸鞘氨醇/1-磷酸鞘氨醇受体3信号通路 |
| KEYWORDS： | picroside Ⅱ； non-small cell lung cancer； proliferation； migration； invasion； sphingosine kinase 1/sphingosine-1- |
| 阅读数： | 94 次 |
| 本月下载数： | 39 次 |
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