Ameliorative effect and mechanism of emodin on infectious preterm rats

CAO Dingya; WU Xiaojuan; FU Tingting; SONG Bing

doi:10.6039/j.issn.1001-0408.2024.21.09

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Ameliorative effect and mechanism of emodin on infectious preterm rats

更新时间：2024-11-08

- Ameliorative effect and mechanism of emodin on infectious preterm rats
- ZHONGGUO YAOFANG Vol. 35, Issue 21, Pages: 2629-2633(2024)
- 作者机构：
  
  1.广州医科大学附属第三医院产前诊断科，广州　510150
  2.广东省产科重大疾病重点实验室，广州　510150
  3.广州医科大学附属第三医院妇产科，广州　510150
- 作者简介：
- 基金信息：
- DOI：10.6039/j.issn.1001-0408.2024.21.09
  CLC： R965
- Published：15 November 2024，
  
  Received：04 June 2024，
  
  Revised：09 August 2024，
- 稿件说明：
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曹定娅,武晓娟,付婷婷等.大黄素对感染性早产大鼠的改善作用及机制 ^Δ[J].中国药房,2024,35(21):2629-2633.

CAO Dingya,WU Xiaojuan,FU Tingting,et al.Ameliorative effect and mechanism of emodin on infectious preterm rats[J].ZHONGGUO YAOFANG,2024,35(21):2629-2633.
曹定娅,武晓娟,付婷婷等.大黄素对感染性早产大鼠的改善作用及机制 ^Δ[J].中国药房,2024,35(21):2629-2633. DOI： 10.6039/j.issn.1001-0408.2024.21.09.

CAO Dingya,WU Xiaojuan,FU Tingting,et al.Ameliorative effect and mechanism of emodin on infectious preterm rats[J].ZHONGGUO YAOFANG,2024,35(21):2629-2633. DOI： 10.6039/j.issn.1001-0408.2024.21.09.

摘要

目的

探究大黄素对感染性早产大鼠的改善作用及机制。

方法

构建感染性早产大鼠模型，将其分成模型组、大黄素组（60 mg/kg，灌胃）、核因子κB（NF-κB）抑制蛋白激酶（IKK）激活组（2 μg pcDNA3.1-IKK重组质粒，尾静脉注射）、大黄素+IKK激活组（灌胃60 mg/kg大黄素+尾静脉注射2 μg pcDNA3.1-IKK重组质粒），每组14只。另取14只受孕雌鼠作为对照组。各组大鼠给予相应药物干预7 d。检测大鼠子宫肌条肌张力和血清中炎症指标[白细胞介素1β（IL-1β）、IL-6、肿瘤坏死因子α（TNF-α）]和氧化应激指标[超氧化物歧化酶（SOD）、丙二醛（MDA）、过氧化氢酶（CAT）]水平；观察大鼠子宫组织病理学形态变化；检测大鼠子宫组织中NOD样受体蛋白3（NLRP3）、剪切型胱天蛋白酶1（cleaved-caspase-1）和IKK/NF-κB抑制蛋白（IκB）/NF-κB信号通路相关蛋白表达水平。

结果

与对照组相比，模型组大鼠子宫平滑肌出现了大量炎症细胞浸润，细胞分布不规则；子宫肌条肌张力和血清中IL-1β、IL-6、TNF-α、MDA水平以及子宫组织中NLRP3、cleaved-caspase-1、IKK、IκB、NF-κB p65蛋白表达水平均显著升高（

＜0.05），血清中SOD、CAT水平均显著降低（

＜0.05）。与模型组相比，大黄素组大鼠子宫平滑肌层炎症细胞浸润现象减轻，各定量指标均明显改善（

＜0.05）；IKK激活组大鼠子宫平滑肌层炎症细胞浸润现象加重，各定量指标均进一步恶化（

＜0.05）。激活IKK可明显减弱大黄素对感染性早产大鼠上述指标的改善作用（

＜0.05）。

结论

大黄素可能通过抑制IKK/IκB/NF-κB信号通路活性，减轻炎症反应和氧化应激，从而改善感染性早产大鼠子宫平滑肌收缩。

Abstract

OBJECTIVE

To explore the ameliorative effect and mechanism of emodin on infectious preterm rats.

METHODS

The infectious preterm rat model was established and divided into model group， emodin group （60 mg/kg， i.g.）， IKK activation group （2 μg pcDNA3.1-IKK recombinant plasmid via tail vein）， emodin+IKK activation group （i.g. 60 mg/kg emodin+2 μg pcDNA3.1-IKK recombinant plasmid via tail vein）， with 14 rats in each group. Another 14 pregnant female rats were set up as control group. Each group received corresponding intervention for 7 days. The muscle tension of the uterine muscle strip， and the indicator levels of serum inflammation [interleukin 1β （IL-1β）， IL-6， tumor necrosis factor α（TNF-α）] and oxidative stress [superoxide dismutase （SOD）， malondialdehyde （MDA）， catalase （CAT）] were detected； the pathological morphological changes of uterine tissue in rats were observed； the protein expressions of NOD-like receptor protein 3 （NLRP3）， cleaved-caspase-1 and IKK/IκB/NF-κB signaling pathway were detected.

RESULTS

Compared with control group， a large number of inflammatory cells infiltrated into the smooth muscle layer of uterus in model group with irregular cell distribution； the uterine muscle strip muscle tone， serum levels of IL-1β， IL-6， TNF-α and MDA， protein expressions of NLRP3， cleaved-caspase-1， IKK， I

κB and NF-κB p65 in uterine tissue were significantly increased in model group， and the serum levels of SOD and CAT were significantly decreased （

＜0.05）. Compared with the model group， the infiltration of inflammatory cells in the uterine smooth muscle layer was reduced in the emodin group， and all quantitative indexes were significantly improved （

＜0.05）； the infiltration of inflammatory cells in the uterine smooth muscle layer was increased in IKK activation group， and all quantitative indexes further deteriorated （

＜0.05）. Activation of IKK could significantly reduce the improvement effect of emodin on the above indexes in infectious preterm rats （

＜0.05）.

CONCLUSIONS

Emodin can relieve inflammation and oxidative stress in infectious preterm rats by inhibiting the IKK/IκB/NF-κB signaling pathway， thus improving uterine smooth muscle contraction.

关键词

大黄素感染性早产IKK/IκB/NF-κB信号通路子宫平滑肌炎症氧化应激

Keywords

infectious pretermIKK/IκB/NF-κB signaling pathwayuterine smooth muscleinflammationoxidative stress

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