| 摘要: |
| ［摘要］ 目的 基于NOD样受体蛋白3（NLRP3）信号通路探讨褪黑素（MT）对子痫前期（PE）滋养层细胞的作用及机制。方法 通过缺氧处理HTR8/SVneo细胞48 h构建PE滋养层细胞模型。CCK8法检测细胞增殖水平，设置对照组（单纯HTR8/SVneo细胞）、PE组、PE+100 μmol/L MT组、PE+500 μmol/L MT组、PE+1 mmol/L MT组。通过流式细胞术检测各组细胞死亡率，采用Transwell实验检测各组细胞的侵袭能力。通过实时荧光定量聚合酶链反应（qRT-PCR）和Western blot实验检测各组细胞中NLRP3信号通路相关因子NLRP3、凋亡相关斑点样蛋白（ASC）、半胱氨酸蛋白酶-1（caspase-1）、白介素-1β（IL-1β）的表达水平。结果 1 mmol/L及以下浓度MT对HTR8/SVneo细胞增殖无显著影响。PE组细胞死亡率显著高于对照组（P<0.05）。与PE组比较，PE+100 μmol/L MT组、PE+500 μmol/L MT组和PE+1 mmol/L MT组细胞死亡率显著降低（P<0.05）。PE组细胞侵袭率显著低于对照组（P<0.05）。与PE组相比，PE+500 μmol/L MT组和PE+1 mmol/L MT组细胞侵袭率显著升高（P<0.05），且细胞侵袭率随MT干预浓度增加呈上升趋势。与对照组相比，PE组细胞NLRP3、ASC、caspase-1、IL-1β的mRNA和蛋白表达显著升高（P<0.05），而MT干预可逆转这一变化。结论 MT能降低PE滋养层细胞的死亡率并增强其侵袭能力，其作用机制可能与抑制NLRP3信号通路相关。 |
| 关键词: 子痫前期 滋养层细胞 褪黑素 NOD样受体蛋白3 |
| DOI：10.3969/j.issn.1674-3806.2026.05.11 |
| 分类号:R 714.244 |
| 基金项目:广西自然科学基金项目（编号：2023GXNSFAA026403）；广西重点研发计划项目（编号：桂科AB22035018） |
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| Study on the role and mechanism of melatonin in trophoblast cells during preeclampsia based on the NLRP3 signaling pathway |
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PAN Ziyang1, LIANG Xuxia2, HU Qiuwen2, QIN Zhiping3, MA Yanhua2, HU Qiongyan2, LU Jun2, LI Hui1, LU Yebin2
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1.Youjiang Medical University for Nationalities, Baise 533000, China; 2.Department of Obstetrics, the People′s Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, China; 3.Department of Obstetrics, Maternity and Child Health Care Hospital of Guangxi Zhuang Autonomous Region, Nanning 530000, China
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| Abstract: |
| ［Abstract］ Objective To study the role and mechanism of melatonin(MT) in trophoblast cells during preeclampsia(PE) based on the NOD-like receptor protein 3(NLRP3) signaling pathway. Methods The model of trophoblast cells during PE was constructed by treating HTR8/SVneo cells for 48 hours under the condition of hypoxia. Cell proliferation levels were detected by using the CCK8 assay. The control group(HTR8/SVneo cells), PE group, PE+100 μmol/L MT group, PE+500 μmol/L MT group and PE+1 mmol/L MT group were set up. The cell mortality rate in each group was detected by using flow cytometry, and the invasive ability of cells in each group was detected by using Transwell assay. The expression levels of NLRP3 signaling pathway-related factor NLRP3, apoptosis-associated speck-like protein containing a CARD(ASC), caspase-1 and interleukin-1β(IL-1β) in the cells of each group were detected by using quantitative real-time polymerase chain reaction(qRT-PCR) and Western blot assay. Results MT at concentrations ≤1 mmol/L had no significant effect on the proliferation of HTR8/SVneo cells. The cell mortality rate in the PE group was significantly higher than that in the control group(P<0.05). Compared with that in the PE group, the cell mortality rate in the PE+100 μmol/L MT group, the PE+500 μmol/L MT group and the PE+1 mmol/L MT group was significantly decreased(P<0.05). The cell invasion rate in the PE group was significantly lower than that in the control group(P<0.05). Compared with that in the PE group, the cell invasion rate in the PE+500 μmol/L MT group and the PE+1 mmol/L MT group was significantly increased(P<0.05), and the cell invasion rate showed an upward trend with the increase of the intervention concentration of MT. Compared with those of the control group, the mRNA and protein expression levels of NLRP3, ASC, caspase-1 and IL-1β in the cells of the PE group were significantly increased(P<0.05), while the intervention of MT could reverse these changes. Conclusion MT can reduce the mortality rate of trophoblast cells during PE and enhance their invasive ability. The mechanisms may be related to the inhibition of the NLRP3 signaling pathway. |
| Key words: Preeclampsia(PE) Trophoblast cells Melatonin NOD-like receptor protein 3(NLRP3) |
