Effect of Jinzhen Oral Liquid on NF-B, MAPK Signaling Pathway in Mice with LPS-induced Acute Lung Injury

ZONG Shao-bo; SUN Lan; LYU Yao-zhong; Zhou Jun; WANG Zhen-zhong; XIAO Wei

doi:10.13422/j.cnki.syfjx.20180733

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Effect of Jinzhen Oral Liquid on NF-B, MAPK Signaling Pathway in Mice with LPS-induced Acute Lung Injury

更新时间：2024-01-04

- Effect of Jinzhen Oral Liquid on NF-B, MAPK Signaling Pathway in Mice with LPS-induced Acute Lung Injury
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 24, Issue 9, Pages: 155-159(2018)
- 作者机构：
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- 基金信息：
- DOI：10.13422/j.cnki.syfjx.20180733
  CLC： R-332;R285.5
- Published：2018
- 稿件说明：
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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：

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.

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