Protective mechanism of liquiritigenin on acute kidney injury in mice

HU Jia-li; CAO Hui; LEI Ru; CUI Juan; CUI Jing

doi:10.11659/jjssx.07E022051

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Protective mechanism of liquiritigenin on acute kidney injury in mice

Basic Research | 更新时间：2023-05-26

- Protective mechanism of liquiritigenin on acute kidney injury in mice
- JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY Vol. 32, Issue 5, Pages: 389-393(2023)
- 作者机构：
  
  1.河北北方学院附属第一医院血液净化科，河北张家口 075000
  2.河北北方学院附属第一医院重症医学科，河北张家口 075000
- 作者简介：
- 基金信息：
- DOI：10.11659/jjssx.07E022051
  CLC： R285.5
- Published：25 May 2023，
  
  Received：14 July 2022，
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胡佳丽,曹卉,雷茹等.甘草素对急性肾损伤小鼠的保护机制研究[J].局解手术学杂志,2023,32(05):389-393.

HU Jia-li,CAO Hui,LEI Ru,et al.Protective mechanism of liquiritigenin on acute kidney injury in mice[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2023,32(05):389-393.
胡佳丽,曹卉,雷茹等.甘草素对急性肾损伤小鼠的保护机制研究[J].局解手术学杂志,2023,32(05):389-393. DOI： 10.11659/jjssx.07E022051.

HU Jia-li,CAO Hui,LEI Ru,et al.Protective mechanism of liquiritigenin on acute kidney injury in mice[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2023,32(05):389-393. DOI： 10.11659/jjssx.07E022051.

摘要

目的

探究甘草素对脂多糖（LPS）诱导的急性肾损伤小鼠的保护作用机制。

方法

将雄性昆明小鼠随机分为对照组、LPS组、LPS+甘草素3.75 mg/kg组、LPS+甘草素7.5 mg/kg组、LPS+甘草素15 mg/kg组和LPS+地塞米松组，每组8只。苏木素-伊红（HE）染色观察肾组织病理变化；全自动生化分析仪检测血清肌酐和血清尿素氮水平。酶联免疫吸附测定（ELISA）检测肾组织中IL-6、IL-1β和TNF-α水平；Western blot检测肾组织中IκBα和NF-κBp65蛋白的磷酸化水平和Toll样受体4（TLR4）、NOD样受体热蛋白结构域相关蛋白3(NLRP3)、Caspase-1、IL-1β蛋白表达水平。

结果

与对照组相比，LPS组小鼠肾组织中有大量炎症细胞浸润，血清肌酐、血清尿素氮、IL-6、IL-1β、TNF-α水平及p-IκBα/IκBα、p-NF-κBp65/NF-κBp65、TLR4、NLRP3、Caspase-1、IL-1β均显著上调，差异均有统计学意义（

0.05）。然而在LPS+甘草素7.5 mg/kg组、LPS+甘草素15 mg/kg组和LPS+地塞米松组中，这些指标变化均发生逆转。

结论

甘草素可能通过抑制NLRP3和NF-κB信号通路缓解LPS诱导的小鼠急性肾损伤。

Abstract

Objective

To explore the protective mechanism of liquiritigenin on lipopolysaccharide （LPS）-induced acute kidney injury in mice.

Methods

Male Kunming mice were randomly divided into the control group，the LPS group，the LPS+liquiritigenin 3.75 mg/kg group，the LPS+liquiritigenin 7.5 mg/kg group，the LPS+liquiritigenin 15 mg/kg group and the LPS+dexamethasone group，with 8 mice in each group.The pathologic changes of kidney tissue were observed by hematoxylin-eosin （HE） staining.The levels of serum creatinine and serum urea nitrogen were detected by automatic biochemical analyzer.The levels of IL-6，IL-1β and TNF-α in renal tissue were detected by enzyme-linked immunosorbent assay （ELISA）.Western blot was used to detect the phosphorylation levels of IκBα and NF-κBp65 protein and the expression levels of Toll-like receptor 4 （TLR4），NOD-like receptor thermal protein domain associated protein 3（NLRP3），Caspase-1 and IL-1β proteins in renal tissue.

Results

Compared with the control group，there were a large number of inflammatory cell infiltration in the renal tissue of mice in the LPS group，and the levels of serum creatinine，serum urea nitrogen，IL-6，IL-1β and TNF-α and p-IκBα/IκBα，p-NF-κBp65/NF-κBp65，TLR4，NLRP3，Caspase-1 and IL-1β were significantly up-regulated，the differences were statistically significant （

0.05）.However，the changes of these indexes were reversed in the LPS+liquiritigenin 7.5 mg/kg group，the LPS+liquiritigenin 15 mg/kg group and the LPS+dexamethasone group.

Conclusion

Liquiritigenin may alleviate LPS-induced acute kidney injury in mice by inhibiting NLRP3 and NF-κB signaling pathways.

关键词

甘草素脂多糖炎症NLRP3通路NF-κB通路

Keywords

liquiritigeninlipopolysaccharideinflammationNLRP3 pathwayNF-κB pathway

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