LPS/CD14结合位点模拟肽对内毒素性大鼠急性肺损伤的治疗作用

徐智; 李昆霖; 陈锐; 钱桂生; 吴国明

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LPS/CD14结合位点模拟肽对内毒素性大鼠急性肺损伤的治疗作用

论著 | 更新时间：2026-01-09

- LPS/CD14结合位点模拟肽对内毒素性大鼠急性肺损伤的治疗作用
- Therapeutic effects of mimic peptide of LBP/CD14 binding site on endotoxin-induced acute lung injure in rats
- 陆军军医大学学报 2012年34卷第24期页码：2469-2473
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  中图分类号： R563.05;R631;R966
- 纸质出版：2012
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徐智,李昆霖,陈锐,钱桂生,吴国明.LPS/CD14结合位点模拟肽对内毒素性大鼠急性肺损伤的治疗作用[J].陆军军医大学学报(原第三军医大学学报),2012,34(24):2469-2473.

　Xu Zhi,Li Kunlin,Chen Rui,Qian Guisheng,Wu Guoming.Therapeutic effects of mimic peptide of LBP/CD14 binding site on endotoxin-induced acute lung injure in rats[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(24):2469-2473.
徐智,李昆霖,陈锐,钱桂生,吴国明.LPS/CD14结合位点模拟肽对内毒素性大鼠急性肺损伤的治疗作用[J].陆军军医大学学报(原第三军医大学学报),2012,34(24):2469-2473. DOI：

　Xu Zhi,Li Kunlin,Chen Rui,Qian Guisheng,Wu Guoming.Therapeutic effects of mimic peptide of LBP/CD14 binding site on endotoxin-induced acute lung injure in rats[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(24):2469-2473. DOI：

摘要

目的观测LPS/CD14结合位点模拟肽（mimic peptides 12

MP12）对内毒素性急性肺损伤大鼠模型的治疗作用。方法将30只Wistar大鼠按随机数字表法分为生理盐水对照组、LPS组和LPS+MP12组（n=10）。另将40只Wistar大鼠分为两组，分别接受与LPS组和LPS+MP12组相同的处理方法，用于观测死亡率。采用LPS静脉注射法复制内毒素性急性肺损伤大鼠模型。LPS+MP12组在接受LPS注射后立即予MP12静脉注射。2 h后抽取静脉血用于检测血浆内毒素浓度。于12 h抽取动脉血，检测动脉血氧分压（PaO

）。24 h后处死各组大鼠，留取右下肺用于病理检查，右上肺匀浆检测TNF-α，留取左肺行支气管肺泡灌洗并分离肺泡巨噬细胞。采用荧光显微镜检测MP12对肺泡巨噬细胞与LPS结合的抑制作用。结果 LPS组及LPS+MP12组的血浆内毒素浓度明显高于生理盐水对照组（P0.01），而LPS组与LPS+MP12组间血浆内毒素浓度无显著差异（P0.05）。LPS组及LPS+MP12组PaO

显著低于生理盐水对照组（P0.01），但LPS+MP12组PaO

显著高于LPS组（P0.01）。LPS+MP12组肺组织TNF-α浓度及病理学评分显著低于LPS组（P0.01）。LPS+MP12组肺泡巨噬细胞与LPS的结合率显著低于LPS组（P0.01）。 LPS+MP12组的72 h死亡率显著低于LPS组（40% vs 75%， P0.01）。结论 LPS/CD14结合位点模拟肽（MP12）能通过阻断内毒素与肺泡巨噬细胞的结合，减轻内毒素导致的肺部炎症及病理损害，显著提高内毒素性急性肺损伤大鼠的动脉血氧分压、减少死亡率。

Abstract

Objective To determine the therapeutic effect of a mimic peptide (mimic peptides 12

MP12) of LBP/CD14 binding site on LPS-induced acute lung injure (ALI) in rat model. Methods Thirty Wistar rats were divided randomly into control group

LPS group and LPS+MP12 group

. Another forty Wistar rats were divided randomly into 2 groups and accepted the same treatment as LPS group and LPS+MP12 group respectively in order to observe the mortality. The rat ALI model was established by intravenous injection of LPS. The rats of LPS+MP12 group accepted MP12 intravenous injection immediately after LPS injection. In 2 h later

blood sample of each group rats were collected to detect the concentration of endotoxin. Arterial blood samples were collected to detect PaO

in 12 h after LPS injection. All rats were executed in 24 h

the right lower lung was embedded for pathological examination

and the right upper lung was used to measure TNFα content. The left lung was used for bronchoalveolar lavage and isolation of alveolar macrophages. The effect of MP12 on the binding between LPS and alveolar macrophages was observed by fluorescence microscopy. Results The endotoxin level in the plasma was significantly higher in LPS group and LPS+MP12 group than control group (P0.01)

but there was no significant difference in the former 2 groups (P0.05). PaO

value was significantly lower in LPS group and LPS+MP12 group than in control group (P0.01)

and

the value was significantly higher in of LPS+MP12 group than LPS group (P0.01). TNFα content in lung tissue and the pathological score were significantly lower in LPS+MP12 group than LPS group (P0.01). The binding between LPS and alveolar macrophages was significantly lower in LPS+MP12 group than LPS group (P0.01). The mortality of LPS+MP12 group were significantly lower than that of LPS group (40% vs 75%

P0.01). Conclusion The mimic peptide of LPS/CD14 binding site blocks the binding between LPS and alveolar macrophages

thereby attenuates the LPS-induced inflammation and pathological damage in the lung

and improves PaO

and mortality of LPS- ALI in rat model.

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