| 摘要: |
| 目的:本研究基于NLRP3信号通路，探究褪黑素（MT）对子痫前期(PE）的影响及作用机制。方法：选用HTR8/SVneo细胞株，通过缺氧处理模拟体外子痫前期细胞模型。CCK8检测细胞检验褪黑素对HTR8/SVneo细胞的影响，选择3个浓度（0.1、0.5、1mM）作为后续处理剂量。将HTR8/SVneo细胞分为：对照组、缺氧处理组、缺氧处理+低剂量褪黑素组、缺氧处理+中剂量褪黑素组、缺氧处理+高剂量褪黑素组。流式检测各组细胞凋亡情况；Transwell检测各组细胞的侵袭能力；qPCR检测各组细胞中炎性小体通路关键因子NLRP3、ASC、Caspase-1、IL-1β的mRNA表达水平；WB检测各组细胞中炎性小体通路关键因子NLRP3、ASC、Caspase-1、IL-1β的蛋白水平。结果：1mM浓度以下的褪黑素对HTR8/SVneo细胞增殖无明显影响。缺氧组细胞凋亡率显著高于对照组，而褪黑素处理组细胞凋亡率显著降低。缺氧组细胞侵袭率显著低于对照组，而褪黑素处理组细胞侵袭率显著升高，且随剂量增加效果更明显。缺氧组NLRP3、ASC、Caspase-1、IL-1β的mRNA和蛋白表达显著升高，而褪黑素处理组这些因子的表达显著降低。结论：褪黑素能减少炎症因子的产生，从而减少子痫前期滋养层细胞的焦亡并增强其侵袭能力，作用机制与通过抑制NLRP3信号通路相关。 |
| 关键词: 子痫前期 褪黑素 NLRP3炎症小体 炎性反应 |
| DOI： |
| 分类号: |
| 基金项目:广西自然科学基金(2023GXNSFAA026403)；广西重点研发计划(桂科AB22035018) |
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| Study on the Role and Mechanism of Melatonin in Preeclamptic Trophoblast Cells Based on the NLRP3 Signaling Pathway |
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pan ziyang
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Youjiang Medical University For Nationalities
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| Abstract: |
| Objective:?This study investigates the impact and mechanism of melatonin on preeclampsia based on the NLRP3 signaling pathway. Methods:?The HTR8/SVneo cell line was used to simulate an in vitro preeclampsia cell model through hypoxia treatment. the CCK8 assay was used to examine the effects of melatonin on HTR8/SVneo cells. Three concentrations (0.1, 0.5, and 1 mM) were selected as the subsequent treatment doses. The HTR8/SVneo cells were divided into: control group, hypoxia group, hypoxia + low-dose melatonin group, hypoxia + medium-dose melatonin group, hypoxia + high-dose melatonin group. Flow cytometry was used to detect the apoptosis of cells in each group; Transwell assay was employed to assess the invasive ability of cells in each group; qPCR was used to detect the mRNA expression levels of key factors in the inflammasome pathway, including NLRP3, ASC, Caspase-1, and IL-1β, in each group of cells; WB was used to detect the protein levels of key factors in the inflammasome pathway, including NLRP3, ASC, Caspase-1, and IL-1β, in each group of cells. Results:?Melatonin at concentrations below 1 mM showed no significant effect on the proliferation of HTR8/SVneo cells. The apoptosis rate in the hypoxia group was significantly higher than that in the control group, while the melatonin-treated group exhibited a significantly reduced apoptosis rate. The cell invasion rate in the hypoxia group was significantly lower than that in the control group, while the cell invasion rate in the melatonin-treated group significantly increased, with the effect becoming more pronounced as the dose increased. The mRNA and protein expressions of NLRP3, ASC, Caspase-1, and IL-1β were significantly increased in the hypoxia group, while these factors were markedly reduced in the melatonin-treated group. Conclusion:?Melatonin can reduce the production of inflammatory factors, thereby decreasing the pyroptosis rate of preeclamptic trophoblast cells and enhancing their invasive ability. The mechanism of action is associated with the inhibition of the NLRP3 signaling pathway. |
| Key words: Preeclampsia Melatonin NLRP3 signaling pathway Inflammatoryresponse |
