Effect of Shenlian Extract on Macrophage Function and Inflammatory Resolution in Lipid Peroxidation Inflammatory Injury Models

Jie YIN; Qi LI; Zheng ZHAO; Qing YANG; Si-si LIU; Yu-jie LI; Ying CHEN; Ya-jie WANG; Xiao-gang WENG; Wei-yan CAI; Xiao-xin ZHU

doi:10.13422/j.cnki.syfjx.20191001

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Effect of Shenlian Extract on Macrophage Function and Inflammatory Resolution in Lipid Peroxidation Inflammatory Injury Models

Pharmacology | 更新时间：2021-02-09

- Effect of Shenlian Extract on Macrophage Function and Inflammatory Resolution in Lipid Peroxidation Inflammatory Injury Models
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 25, Issue 10, Pages: 26-32(2019)
- 作者机构：
  
  1.首都医科大学　中医药学院，北京　 100069；
  2.中国中医科学院　中药研究所，北京　 100700
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.20191001
  CLC： R2-0; R22; R285.5
- Received：11 January 2019，
  
  Published Online：11 February 2019，
  
  Published：20 May 2019
- 稿件说明：
移动端阅览
Jie YIN, Qi LI, Zheng ZHAO, et al. Effect of Shenlian Extract on Macrophage Function and Inflammatory Resolution in Lipid Peroxidation Inflammatory Injury Models[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(10): 26-32.
DOI：

Jie YIN, Qi LI, Zheng ZHAO, et al. Effect of Shenlian Extract on Macrophage Function and Inflammatory Resolution in Lipid Peroxidation Inflammatory Injury Models[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(10): 26-32. DOI： 10.13422/j.cnki.syfjx.20191001.

摘要

目的：

研究参莲(SL)提取物在脂质过氧化炎症损伤模型中，对巨噬细胞功能的作用和促进炎症消散的药效和药理机制。

方法：

利用氧化低密度脂蛋白(ox-LDL)体外诱导小鼠巨噬细胞RAW264.7细胞和人单核细胞THP-1造成脂质过氧化损伤模型，酶联免疫吸附测定(ELISA)检测不同质量浓度的SL提取物(2.5，5.0，10.0，20.0 mg·L

－1

)对巨噬细胞肿瘤坏死因子-

(TNF-

)，白细胞介素-1

(IL-1

)，单核细胞趋化蛋白-1(MCP-1)的含量；流式细胞术检测巨噬细胞泡沫化形成；transwell实验检测SL提取物对THP-1趋化功能的影响；以及用蛋白免疫印迹法(Western blot)检测诱导型一氧化氮合酶(iNOS)，炎症消散因子5脂氧合酶(ALOX5)以及对核转录因子-

B(NF-

B)信号通路中的磷酸化p65(p-p65)和磷酸化I

K(p-I

K)蛋白表达情况。

结果：

与正常组比较，ox-LDL提高M1型巨噬细胞标志物TNF-

，IL-1

，iNOS的表达(

0.01)，抑制M2型标志物IL-10的表达，促进泡沫细胞形成(

0.01)，诱导THP-1向ox-LDL趋化，提高MCP-1分泌量(

0.01)，抑制ALOX5的表达。与模型组比较，SL提取物可以降低TNF-

，IL-1

，iNOS的表达(

0.01)，提高IL-10的表达(

0.05)；能显著降低巨噬细胞吞噬脂质后泡沫化的形成(

0.01)；能降低THP-1细胞MCP-1的分泌(

0.01)，减少趋化的细胞数目(

0.01)；促进炎症消散因子ALOX5的升高(

0.05)，同时抑制p65和I

K磷酸化表达(

0.01)。

结论：

在脂质过氧化炎症损伤模型中，SL提取物具有诱导巨噬细胞M2极化，抑制巨噬细胞对ox-LDL的趋化和泡沫化的形成，提高ALOX5表达，促进炎症消散，从而改善脂质过氧化炎症损伤状态，上述功能与抑制NF-

B信号通路中p65和I

K磷酸化水平有关。

Abstract

Objective:

To study the effect of Shenlian extract (SL extract) on macrophage function and inflammatory resolution in lipid peroxidation inflammatory injury models.

Method:

The effects of different concentrations of SL extract (2.5

5.0

10.0

20.0 mg·L

-1

) on the polarization type

foam formation and chemotactic function of macrophages were detected with RAW264.7 cells induced by oxidized low-density lipoprotein(ox-LDL). Western blot was used to detect pro-inflammatory resolution factor arachidonate 5-lipoxygenase(ALOX5) and inducible inducible nitric oxide synthase(iNOS)

and phosphorylated p65 (p-p65) and phosphorylated I

K (p-I

K) in nuclear factor(NF)-

B related signaling pathways.

Result:

Compared with the control group

ox-LDL enhanced the expressions of M1 macrophage markers TNF-

IL-1

iNOS (

0.01)

inhibited the expressions of IL-10 of M2 markers

promoted foam cell formation (

0.01)

induced THP-1 chemotaxis ability

increased the content of MCP-1 (

0.01)

and inhibited the expression of ALOX5.Compared with the model group

SL extract reduced the expressions of TNF-

IL-1

and iNOS (

0.01)

increased the expression of IL-10 (

0.05)

and down-regulated the formation of foam of macrophages (

0.01). In transwell assay

SL extract obviously decreased the MCP-1 secretion and the number of chemotaxis cells (

0.01)

and promoted the increase of the inflammatory resolution factor ALOX5.The phosphorylation of p65 and I

K was inhibited significantly (

0.01).

Conclusion:

In the inflammatory damage model of lipid peroxidation

SL extract can regulate the polarization of macrophage

inhibit the chemotaxis and foaming of ox-LDL

increase the inflammatory resolution molecular expression

and improve the state of lipid peroxidation

which may be related to the inhibition of NF-

B signaling pathway.

关键词

Keywords

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