Relationship between expression of autophagy regulation interleukin-33 and the pathogenesis of preeclampsia

Shi Shuming; Xu Fang; Zhang Hua

doi:10.13406/j.cnki.cyxb.000973

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Relationship between expression of autophagy regulation interleukin-33 and the pathogenesis of preeclampsia

更新时间：2024-01-17

- Relationship between expression of autophagy regulation interleukin-33 and the pathogenesis of preeclampsia
- Journal of Chongqing Medical University Vol. 41, Issue 7, Pages: 663-668(2016)
- 作者机构：
  
  1. 重庆医科大学附属第一医院妇产科
  2. 重庆医科大学附属第一医院急诊医学科&重症医学科
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.000973
  CLC： R714.244
- Published：2016，
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[1]石书明,徐昉,张华.自噬调节白介素-33的表达与子痫前期发病机制的关系[J].重庆医科大学学报,2016,41(07):663-668.

Shi Shuming, Xu Fang, Zhang Hua. Relationship between expression of autophagy regulation interleukin-33 and the pathogenesis of preeclampsia. [J]. Journal of Chongqing Medical University 41(7):663-668(2016)
[1]石书明,徐昉,张华.自噬调节白介素-33的表达与子痫前期发病机制的关系[J].重庆医科大学学报,2016,41(07):663-668. DOI： 10.13406/j.cnki.cyxb.000973.

Shi Shuming, Xu Fang, Zhang Hua. Relationship between expression of autophagy regulation interleukin-33 and the pathogenesis of preeclampsia. [J]. Journal of Chongqing Medical University 41(7):663-668(2016) DOI： 10.13406/j.cnki.cyxb.000973.

摘要

目的:探究白介素-33（interleukin-33

IL-33）在子痫前期（preeclampsia

PE）胎盘中的表达以及自噬通过调节IL-33的表达参与PE发病的分子机制。方法:应用免疫组化法及Western blot检测PE患者与正常妊娠胎盘中IL-33

微管相关蛋白LC3（LC3）的表达

应用Western blot检测PE患者与正常妊娠胎盘中IL-33受体ST2和核转录因子-κB（nuclear factor

NF-κB）的表达。使用3-Methyladenine（3-MA）、巴佛洛霉素A1（bafilomycin A1

BAF）处理人类绒毛膜外滋养细胞株HTR8/SVneo

检测IL-33、ST2和NF-κB蛋白表达情况以及自噬水平的高低。结果:（1）Western blot检测结果显示IL-33平均吸光度（absorbance

A）值PE组低于对照组（t=2.830

P=0.010）

LC3B/A平均A值PE组高于对照组（t=3.470

P=0.005）

ST2蛋白表达PE组高于对照组（t=2.650

P=0.026）

NF-κB表达水平PE组高于对照组（t=3.180

P=0.005）;（2）BAF处理HTR8/SVneo细胞株

IL-33蛋白水平较正常对照组明显降低（ta=3.740

Pa=0.006）

LC3B/A比值水平较二甲基甲砜（dimethyl sulphoxide

DMSO）组明显升高（td=2.500

Pd=0.032）。3-MA对IL-33、NF-κB以及自噬水平的表达情况影响不明显。结论:过度自噬可能降低IL-33水平

导致IL-33抗炎作用减弱

进而出现过度炎症反应

并且这一过程与PE的发病存在一定关系。

Abstract

Objective:To characterize the deregulation of interleukin-33(IL-33)expression which regulated by autophagy in the pathological process of preeclampsia(PE). Methods:The expressions of IL-33 protein and autophagy were detected in placentas of normal term and pregnancies complicated with PE by immunohistochemistry and Western blot. The levels of ST2

specific receptor of IL-33

and nuclear factor(NF-κB)were tested in placentas of normal term and pregnancies complicated with PE by Western blot.The autophagy pharmacological cell model was built in vitro by using HTR8/SVneo cell line which treated with 3-methyladenine(the inhibition of autophagy)and bafilomycin A1(the inhibition of autophagy body material degradation);then the expressions of IL-33

ST2 and NF-κB were detected by Western blots. Results:The expressions of IL-33 protein were reduced

expressions of LC3B/A were increased

expressions of ST2 protein and NF-κB were increased in placentas of pregnancies complicated with PE than in placentas of normal term(t=2.830

P=0.010;t=3.470

P=0.005;t=2.650

P=0.026;t=3.180

P=0.005). In addition

BAF treatment exerted negative influence on the level of IL-33 in HTR8/SVneo cells(ta=3.740

Pa=0.006)

however

3-MA treatment had no significant function.Conclusion:Autophagy plays a role in the pathophysiology mechanism of PE through the down-regulating the levels and anti-inflammatory effects of IL-33.

关键词

白介素-33子痫前期自噬滋养细胞

Keywords

interleukin-33preeclampsiaautophagytrophoblast

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