金振口服液对LPS致急性肺损伤模型小鼠NF-B，MAPK信号通路的影响

宗绍波; 孙兰; 吕耀中; 周军; 王振中; 萧伟

doi:10.13422/j.cnki.syfjx.20180733

您当前的位置：

首页 >

文章列表页 >

金振口服液对LPS致急性肺损伤模型小鼠NF-B，MAPK信号通路的影响

药理 | 更新时间：2024-01-04

- 金振口服液对LPS致急性肺损伤模型小鼠NF-B，MAPK信号通路的影响
- Effect of Jinzhen Oral Liquid on NF-B, MAPK Signaling Pathway in Mice with LPS-induced Acute Lung Injury
- 中国实验方剂学杂志 2018年24卷第9期页码：155-159
- 作者机构：
- 作者简介：
- 基金信息：
  
  国家“重大新药创制”科技重大专项（2013ZX09402203）
- DOI：10.13422/j.cnki.syfjx.20180733
  中图分类号： R-332;R285.5
- 纸质出版日期：2018
- 稿件说明：
移动端阅览
宗绍波, 孙兰, 吕耀中, 等. 金振口服液对LPS致急性肺损伤模型小鼠NF-B，MAPK信号通路的影响[J]. 中国实验方剂学杂志, 2018,24(9):155-159.

ZONG Shao-bo, SUN Lan, LYU Yao-zhong, et al. Effect of Jinzhen Oral Liquid on NF-B, MAPK Signaling Pathway in Mice with LPS-induced Acute Lung Injury[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(9): 155-159.
宗绍波, 孙兰, 吕耀中, 等. 金振口服液对LPS致急性肺损伤模型小鼠NF-B，MAPK信号通路的影响[J]. 中国实验方剂学杂志, 2018,24(9):155-159. DOI： 10.13422/j.cnki.syfjx.20180733.

ZONG Shao-bo, SUN Lan, LYU Yao-zhong, et al. Effect of Jinzhen Oral Liquid on NF-B, MAPK Signaling Pathway in Mice with LPS-induced Acute Lung Injury[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(9): 155-159. DOI： 10.13422/j.cnki.syfjx.20180733.

摘要

目的：探讨金振口服液（JZKFY）对脂多糖（LPS）致急性肺损伤（ALI）模型小鼠的影响及其分子水平作用机制。方法：小鼠随机分为正常组、模型组、醋酸地塞米松组、金振口服液高、中、低（4.4，2.2，1.1 g · kg-1）剂量组，各给药组给予相应剂量药物，正常组和模型组灌胃同等剂量的生理盐水，1次/d，连续7 d后，模型组及药物组小鼠腹腔注射LPS（10 mg · kg-1）复制急性肺损伤小鼠模型，正常组腹腔注射同等剂量的生理盐水。6 h后采集小鼠肺组织，测定左肺湿/干质量比（W/D）；酶联免疫吸附法（ELISA）检测肺组织中肿瘤坏死因子-α（TNF-α），白细胞介素（IL）-1β；蛋白免疫印迹法（Western blot）测定肺组织中p65，IκBα，ERK1/2，p38蛋白及其磷酸化蛋白表达水平。结果：与正常组比较，模型组小鼠W/D显著升高（P<0.01），肺组织中TNF-α，IL-1β水平显著升高（P<0.01），p65，IκBα，ERK1/2，p38蛋白磷酸化水平显著上调（P<0.01）。与模型组比较，金振口服液低、高剂量及地塞米松组W/D显著降低（P<0.05，P<0.01）；金振口服液各剂量组及地塞米松组肺组织中TNF-α，IL-1β水平显著降低；金振口服液各剂量组及地塞米松组p65，IκBα，p38蛋白磷酸化水平显著下调（P<0.05，P<0.01），金振口服液高剂量、地塞米松组ERK1/2蛋白磷酸化水平显著下调（P<0.05，P<0.01）。结论：金振口服液能够有效改善LPS诱导的ALI肺组织间质性水肿及降低致炎细胞因子的含量，其作用机制与抑制p65，IκBα，ERK1/2，p38多个靶蛋白磷酸化，从而阻断核转录因子-κB（NF-κB），丝裂原活化蛋白激酶（MAPK）炎症通路的信号传导密切相关。

Abstract

Objective: To explore the effect and mechanism of Jinzhen oral liquid (JZOL) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) model in mice. Method: Mice were randomly divided into normal control group

model group

dexamethasone group (DEX)

JZOL high (JZOLG)

medium (JZOLZ) and low (JZOLD) dose (4.4

2.2

1.1 g · kg-1) groups. Corresponding dose of medicine was given in the treatment groups

and the mice in normal group and model group received the same dose of normal saline

once a day for 7 days. Then the ALI models were induced by intraperitoneal injection of LPS (10 mg · kg-1)

while the mice in normal group received intraperitoneal injection of the same dose of normal saline. Six hour later

the lung tissues were taken; left lung wet-to-dry ratio (W/D) was measured; tumor necrosis factor (TNF)-α

and interleukin(IL)-1β in lung tissues were detected by enzyme-linked immunosorbent assay (ELISA); the protein expression levels of p65

IκBα

ERK1/2

p38 protein and their phosphorylation levels in lung tissues were detected by Western blot. Result: As compared with the normal group

the W/D

levels of TNF-α

IL-1β and the phosphorylation expression levels of p65

IκB

p38 protein were increased in the model group(P<0.01). As compared with the model group

the W/D was significantly decreased in JZOLD

JZOLG and DEX groups; the levels of TNF-α and IL-1β were decreased significantly

and the phosphorylation expression levels of p65

IκB

p38 protein were significantly down-regulated in JZOLG

JZOLZ

JZOLD

and DEX groups(P<0.05

P<0.01); and the phosphorylation expression level of ERK1/2 was significantly down-regulated in JZOLG and DEX groups(P<0.05

P<0.01). Conclusion: JZOLY can effectively improve the interstitial edema of the lung tissues and reduce inflammatory cytokines in mice with LPS-induced ALI. The mechanism is closely associated with inhibiting the phosphorylation levels of p65

IκBα

ERK1/2 and p38

blocking nuclear transcription factor-kappa B (NF-κB) and mitogen activated protein kinase (MAPK) inflammatory pathway.

关键词

Keywords

references

浏览量

下载量

CSCD

文章被引用时，请邮件提醒。

提交

工具集

关联资源

中药调控氧化应激干预急性肺损伤的研究进展

清瘟败毒饮及其活性成分防治肺损伤的研究进展

基于p38 MAPK/NF-κB信号通路探讨麻杏苦甘汤对油酸诱导的急性肺损伤大鼠炎症反应及细胞凋亡的影响

中药通过调节NLRP3炎症小体治疗急性肺损伤的研究进展

基于花生四烯酸代谢途径探讨炎调方治疗脂多糖所致急性肺损伤的机制