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[1]沈冬青,廖心成,伍曉妍,等.高遷移率族蛋白-1通過(guò)TLR4/eNOS信號(hào)通路介導(dǎo)膿毒癥小鼠血腦屏障損傷[J].福建醫(yī)藥雜志,2024,46(06):67-71.[doi:10.20148/j.fmj.2024.06.021]
　SHEN Dongqing,LIAO Xincheng,WU Xiaoyan,et al.HMGB1 mediates blood-brain barrier disruption in septic mice via TLR4/eNOS signaling pathway[J].FUJIAN MEDICAL JOURNAL,2024,46(06):67-71.[doi:10.20148/j.fmj.2024.06.021]
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高遷移率族蛋白-1通過(guò)TLR4/eNOS信號(hào)通路介導(dǎo)膿毒癥小鼠血腦屏障損傷()
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《福建醫(yī)藥雜志》[ISSN:1002-2600/CN:35-1071/R]

卷:
46
期數(shù):
2024年06期
頁(yè)碼:
67-71
欄目:
基礎(chǔ)研究
出版日期:
2024-11-15

文章信息/Info

Title:
HMGB1 mediates blood-brain barrier disruption in septic mice via TLR4/eNOS signaling pathway
文章編號(hào):
1002-2600(2024)06-0067-05
作者:
沈冬青; 廖心成; 伍曉妍; 姚玉笙
福建醫(yī)科大學(xué)省立臨床醫(yī)學(xué)院, 福州 350001
Author(s):
SHEN Dongqing;  LIAO Xincheng;  WU Xiaoyan;  YAO Yusheng
Department of Anesthesiology, Shengli Clinical Medical College of Fujian Medical University, Fuzhou, Fujian 350001, China
關(guān)鍵詞:
認(rèn)知功能障礙;  高遷移率族蛋白-1;  血腦屏障;  膿毒癥腦病
Keywords:
cognitive dysfunction;  high mobility group box-1 protein;  blood-brain barrier;  sepsis-associated encephalopathy
分類號(hào):
R3
DOI:
10.20148/j.fmj.2024.06.021
文獻(xiàn)標(biāo)志碼:
A
摘要:
目的 探討高遷移率族蛋白-1(HMGB1)在膿毒性腦病發(fā)病機(jī)制中的作用。方法 將成年雄性C57BL/6J小鼠隨機(jī)分為4組:假手術(shù)(Sham)組(溶劑預(yù)處理1 d,假手術(shù))、Sham + 炎性色素(ICM)組(炎性色素10 mg/kg預(yù)處理1天,假手術(shù))、盲腸結(jié)扎穿孔(CLP)組(溶劑預(yù)處理1天,CLP建模)和CLP + ICM組(炎性色素10 mg/kg預(yù)處理1天,CLP建模)。采用Morris水迷宮評(píng)估小鼠空間記憶功能,曠場(chǎng)實(shí)驗(yàn)評(píng)估自主活動(dòng)能力。術(shù)后第1天,通過(guò)血腦屏障滲漏實(shí)驗(yàn)評(píng)估血腦屏障完整性; Western blot檢測(cè)大腦皮質(zhì)緊密連接蛋白(ZO-1、Occludin和Claudin-5)以及Toll樣受體4(TLR4)、內(nèi)皮一氧化氮合酶(eNOS)的表達(dá)水平。結(jié)果 與CLP組相比,CLP + ICM組水迷宮定位航行實(shí)驗(yàn)潛伏期縮短,空間探索實(shí)驗(yàn)?zāi)繕?biāo)象限停留時(shí)間和平臺(tái)穿越次數(shù)增加。術(shù)后第1天血腦屏障滲透率降低; 大腦皮質(zhì)ZO-1、Occludin、Claudin-5表達(dá)上調(diào); TLR4、eNOS表達(dá)水平下調(diào)。結(jié)論 HMGB1可能通過(guò)激活TLR4/eNOS通路介導(dǎo)膿毒癥小鼠血腦屏障損傷, 進(jìn)而促進(jìn)膿毒性腦病的發(fā)生。
Abstract:
Objective To investigate the role of high mobility group box-1(HMGB1)in the pathogenesis of sepsis-associated encephalopathy(SAE). Methods Adult male C57BL/6J mice were randomly divided into 4 groups: Sham(vehicle pretreatment for 1 day, sham operation), Sham+ICM(Inflachromene 10 mg/kg pretreatment for 1 day, sham operation), cecal ligation and puncture(CLP)(vehicle pretreatment for 1 day, cecal ligation and puncture CLP modeling), and CLP+ICM(Inflachromene 10 mg/kg pretreatment for 1 day, CLP modeling). Morris water maze was used to evaluate spatial memory function, and open field test was used to assess spontaneous activity. On the first day after surgery, blood-brain barrier permeability was evaluated through leakage experiments. Western blot was used to detect the expression levels of tight junction proteins(ZO-1, Occludin, and Claudin-5)in the cerebral cortex, as well as Toll-like receptor 4(TLR4)and endothelial nitric oxide synthase(eNOS). Results Compared with the CLP group, the CLP+ICM group exhibited shortened latency in the water maze positioning navigation experiment, increased target quadrant dwelling time, and increased platform crossing times in the spatial probe test. On the first day after surgery, blood-brain barrier permeability was reduced; the expression of ZO-1, Occludin, and Claudin-5 in the cerebral cortex was upregulated; and the expression levels of TLR4 and eNOS were downregulated. Conclusion HMGB1 may mediate blood-brain barrier damage in septic mice by activating the TLR4/eNOS pathway, thereby promoting the occurrence of SAE.

參考文獻(xiàn)/References:

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備注/Memo

備注/Memo:
基金項(xiàng)目:福建省衛(wèi)生計(jì)生中青年骨干人才培養(yǎng)項(xiàng)目(2016-ZQN-7); 福建省衛(wèi)生健康科技計(jì)劃項(xiàng)目(2022CXA007)
通信作者:姚玉笙,Email:[email protected]
更新日期/Last Update: 2024-11-15