[1]陈鹤翔,何 旋,吴晓静,等.脂多糖诱导大鼠脓毒症相关心肺损伤模型的构建及评价[J].医学信息,2023,36(19):75-79.[doi:10.3969/j.issn.1006-1959.2023.19.015]
　CHEN He-xiang,HE Xuan,WU Xiao-jing,et al.Construction and Evaluation of Lipopolysaccharide-induced Sepsis-related Myocardial Injury and Lung Injury Model in Rats[J].Journal of Medical Information,2023,36(19):75-79.[doi:10.3969/j.issn.1006-1959.2023.19.015]
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脂多糖诱导大鼠脓毒症相关心肺损伤模型的构建及评价()
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医学信息[ISSN:1006-1959/CN:61-1278/R]

卷:
36卷
期数:
2023年19期
页码:
75-79
栏目:
论著
出版日期:
2023-10-01

文章信息/Info

Title:
Construction and Evaluation of Lipopolysaccharide-induced Sepsis-related Myocardial Injury and Lung Injury Model in Rats
文章编号:
1006-1959（2023）19-0075-05
作者:
陈鹤翔; 何 旋; 吴晓静; 等
（1.武汉大学人民医院麻醉科，湖北 武汉 430060；2.咸丰县人民医院麻醉科，湖北 咸丰 445699）
Author(s):
CHEN He-xiang; HE Xuan; WU Xiao-jing; et al.
(1.Department of Anesthesiology,Renmin Hospital,Wuhan University,Wuhan 430060,Hubei,China; 2.Department of Anesthesiology,Xianfeng County People’s Hospital,Xianfeng 445600,Hubie,China)
关键词:
脂多糖; 脓毒症; 心肌损伤; 肺损伤
Keywords:
Lipopolysaccharide; Sepsis; Myocardial injury; Lung injury
分类号:
R459.7
DOI:
10.3969/j.issn.1006-1959.2023.19.015
文献标志码:
A
摘要:
目的 观察脂多糖（LPS）诱导大鼠脓毒症相关心肺损伤情况，为构建大鼠脓毒症相关器官损伤模型并研究脓毒症相关疾病提供有效的实验手段。方法 采用随机数字表法将SPF级雄性Sprague-Dawley大鼠分为对照组（Control组）和LPS模型组（LPS组）两组，每组10只。建立脂多糖诱导的大鼠脓毒症模型。LPS组腹腔注射LPS（10 mg/kg）；C组腹腔注射等量生理盐水。注射后24 h行超声心动图检查心功能。留取心肺组织标本和血标本。ELISA法检测血清中肿瘤坏死因子α（TNF-α）、白介素1β（IL-1β）、白介素6（IL-6）、高迁移率族蛋白B1（HMGB1）、肌钙蛋白I（cTnI）和脑钠肽（BNP）的水平。检测每组大鼠肺组织湿重与干重的比值（W/D）。HE染色观察心肺组织病理改变并进行肺损伤评分。结果 与C组比较，脂多糖腹腔注射后LPS组大鼠于24 h内死亡4只，生存率降低（P＜0.05）；造模24 h后LPS组大鼠血清中TNF-α、IL-1β、IL-6、HMGB1含量升高（P＜0.05），炎症反应重；左室射血分数降低，心室舒张功能及室壁运动幅度减退，血清中cTnI和BNP含量升高（P＜0.05），HE染色也可见心肌细胞水肿、坏死及炎症细胞浸润等明显损伤；肺损伤评分和肺组织W/D比值升高（P＜0.05）。同时，HE染色可见肺泡间隔增宽、间质充血水肿以及炎症细胞浸润明显，肺损伤显著。结论 实验成功建立脂多糖诱导大鼠脓毒症及相关心肺损伤模型，该方法稳定、可靠，可为探讨脓毒症相关疾病提供模型基础。
Abstract:
Objective To observe the sepsis-related myocardial injury and lung injury induced by lipopolysaccharide (LPS) in rats, and to provide an effective experimental method for the construction of sepsis-related organ injury model in rats and the study of sepsis-related diseases.Methods SPF male Sprague-Dawley rats were divided into two groups with random number table method (n=10): Control group (group C), LPS model group (group LPS). Establish a rat model of sepsis induced by LPS. Rats in group LPS were intraperitoneally injected with LPS (10 mg/kg); rats in group C were intraperitoneally injected with an equivalent amount of saline solution. After 24 h, cardiac function was measured with echocardiography. Then, blood samples, cardiac and lung tissue samples were collected. Serum tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), IL-6, high mobility group box-1 (HMGB1), cardiac troponin I (cTnI) and brain natriuretic peptide (BNP) were detected by ELISA. Wet/dry weight ratio (W/D) in lung tissues was detected. Myocardial and pulmonary pathological changes and lung injury score were observed through HE staining.Results Compared with group C, 4 rats in group LPS died within 24 h of modeling and the survival rate was significantly decreased (P<0.05). After 24 hours of modeling, the levels of serum TNF-α, IL-1β, IL-6 and HMGB1 in LPS group increased (P<0.05), and the inflammatory response was severe. Left ventricular ejection fraction decreased, ventricular diastolic function and wall motion amplitude decreased, serum cTnI and BNP levels increased (P<0.05), HE staining also showed obvious damage such as myocardial cell edema, necrosis and inflammatory cell infiltration. Lung injury score and lung tissue W/D ratio increased (P<0.05). At the same time, HE staining showed widened alveolar septum, interstitial congestion and edema, obvious infiltration of inflammatory cells, and significant lung injury.Conclusion The model of lipopolysaccharide-induced sepsis and related myocardial injury and lung injury in rats is successfully established. This method is stable and reliable, and can provide a model basis for exploring sepsis-related diseases.

参考文献/References:

[1]Fernando SM,Rochwerg B,Seely A.Clinical implications of the third international consensus definitions for sepsis and septic shock (Sepsis-3)[J].CMAJ,2018,190(36):1058-1059.[2]Singer M,Deutschman CS,Seymour CW,et al.The third international consensus definitions for sepsis and septic shock (Sepsis-3)[J].JAMA,2016,315(8):801-810.[3]Hubbard WJ,Choudhry M,Schwacha MG,et al.Cecal ligation and puncture[J].Shock,2005,24 Suppl 1:52-57.[4]Remick DG,Ward PA.Evaluation of endotoxin models for the study of sepsis[J].Shock,2005,24 Suppl 1:7-11.[5]Rosier F,Nunez NF,Torres M,et al.Transcriptional response in a sepsis mouse model reflects transcriptional response in sepsis patients[J].Int J Mol Sci,2022,23(2):821.[6]Smith KM,Mrozek JD,Simonton SC,et al.Prolonged partial liquid ventilation using conventional and high-frequency ventilatory techniques: gas exchange and lung pathology in an animal model of respiratory distress syndrome[J].Crit Care Med,1997,25(11):1888-1897.[7]Evans L,Rhodes A,Alhazzani W,et al.Surviving sepsis campaign: international guidelines for management of sepsis and septic shock 2021[J].Crit Care Med,2021,49(11):1063-1143.[8]Song W,Zhang T,Yang N,et al.Inhibition of microRNA miR-122-5p prevents lipopolysaccharide-induced myocardial injury by inhibiting oxidative stress, inflammation and apoptosis via targeting GIT1[J].Bioengineered,2021,12(1):1902-1915.[9]Assinger A,Schrottmaier WC,Salzmann M,et al.Platelets in sepsis: an update on experimental models and clinical data[J].Front Immunol,2019,10:1687.[10]Stortz JA,Raymond SL,Mira JC,et al.Murine models of sepsis and trauma: can we bridge the gap?[J].ILARJ,2017,58(1):90-105.[11]Huang J,Peng W,Zheng Y,et al.Upregulation of UCP2 expression protects against LPS-induced oxidative stress and apoptosis in cardiomyocytes[J].Oxid Med Cell Longev,2019,2019:2758262.[12]Yang X,Sun J,Sun F,et al.TRIM31 promotes apoptosis via TAK1-mediated activation of NF-kappaB signaling in sepsis-induced myocardial dysfunction[J].Cell Cycle,2020,19(20):2685-2700.[13]Hanna A,Frangogiannis NG.Inflammatory cytokines and chemokines as therapeutic targets in heart failure[J].Cardiovasc Drugs Ther,2020,34(6):849-863.[14]Shang X,Lin K,Yu R,et al.Resveratrol Protects the Myocardium in Sepsis by Activating the Phosphatidylinositol 3-Kinases (PI3K)/AKT/Mammalian Target of Rapamycin (mTOR) Pathway and Inhibiting the Nuclear Factor-kappaB (NF-kappaB) Signaling Pathway[J].Med Sci Monit,2019,25:9290-9298.[15]Mannes M,Schmidt CQ,Nilsson B,et al.Complement as driver of systemic inflammation and organ failure in trauma, burn, and sepsis[J].Semin Immunopathol,2021,43(6):773-788.[16]Lafon T,Appert A,Hadj M,et al.Comparative early hemodynamic profiles in patients presenting to the emergency department with septic and nonseptic acute circulatory failure using focused echocardiography[J].Shock,2020,53(6):695-700.[17]L’Heureux M,Sternberg M,Brath L,et al.Sepsis-induced cardiomyopathy: a comprehensive review[J].Curr Cardiol Rep,2020,22(5):35.[18]Thygesen K,Alpert JS,Jaffe AS,et al.Fourth universal definition of myocardial infarction (2018)[J].J Am Coll Cardiol,2018,72(18):2231-2264.[19]Shang C.B-type natriuretic peptide-guided therapy for perioperative medicine?[J].Open Heart,2014,1(1):105.[20]Tu Y,Li X,Fu Y,et al.Isocorydine Ameliorates IL-6 Expression in Bone Marrow-Derived Macrophages and Acute Lung Injury Induced by Lipopolysaccharide[J].Int J Mol Sci,2023,24(5):4629.

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更新日期/Last Update: 1900-01-01