中文English
ISSN 1001-5256 (Print)
ISSN 2097-3497 (Online)
CN 22-1108/R

Changes and formation mechanism of plasma endothelial microparticles in patients with acute pancreatitis

DOI: 10.3969/j.issn.1001-5256.2022.09.027
More Information
  • Corresponding author: MEI Qiao, meiqiao@hotmail.com(ORCID: 0000-0002-0635-6564)
  • Received Date: 2022-01-17
  • Accepted Date: 2022-02-20
  • Published Date: 2022-09-20
  •   Objective  To investigate the changes and formation mechanism of plasma endothelial microparticles (EMPs) in patients with acute pancreatitis (AP).  Methods  Blood samples were collected from 60 patients with AP who were treated in The First Affiliated Hospital of Anhui Medical University from August 2020 to June 2021, and these patients were divided into mild acute pancreatitis (MAP) group with 23 patients, moderate-severe acute pancreatitis (MSAP) group with 23 patients, and severe acute pancreatitis (SAP) group with 14 patients; 20 individuals who underwent physical examination were enrolled as control group.Differential centrifugation was used to obtain platelet-poor plasma, flow cytometry was used to measure the level of CD31+CD41-EMPs, and ELISA was used to measure the levels of endothelin-1(ET-1), von Willebrand factor (vWF), nitric oxide (NO), and vascular cell adhesion molecule-1(VCAM-1).HUVECs were stimulated by the plasma of AP patients, and then flow cytometry and qRT-PCR were used to measure the changes in EMPs, reactive oxygen species (ROS), and mitochondrial membrane potential and the expression of endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), intercellular adhesion molecule-1(ICAM-1), VCAM-1, NADPH oxidase, and P-selectin.A one-way analysis of variance was used for comparison of normally distributed continuous data between multiple groups, and the least significant difference t-test was used for further comparison between two groups.The Kruskal-Wallis H test was used for comparison of non-normally distributed continuous data between groups and within each group.The chi-square test was used for comparison of categorical data between groups, and the Pearson correlation test was used for correlation analysis.  Results  Compared with the control group, the MAP, MSAP, and SAP groups had a significant increase in the level of EMPs (all P < 0.05).Compared with the MAP and MSAP groups, the SAP group had a significant increase in the level of EMPs (both P < 0.05).In the patients with AP, the level of EMPs was negatively correlated with Acute Physiology and Chronic Health Evaluation Ⅱ score, Bedside Index for Severity in Acute Pancreatitis, Ranson score, CT score, and C-reactive protein (r=0.686 2, 0.777 3, 0.713 8, 0.771 8, and 0.473 9, all P < 0.01).Compared with the control group, the MAP, MSAP, and SAP groups had significant increases in the levels of ET-1, vWF, and VCAM-1 and a significant reduction in the level of NO (all P < 0.05).Compared with the control group, the MSAP and SAP groups had the plasma that promoted the release of a large amount of EMPs (both P < 0.05).Compared with the control group, all the other groups, except the MAP group in terms of VCAM-1 and eNOS, had significant increases in the mRNA expression levels of eNOS, iNOS, ICAM-1, P-selectin, VCAM-1, and NADPH oxidase (all P < 0.05).Compared with the HC group, the MAP, MSAP, and SAP groups and the LPS group had a significant increase in the level of ROS and a significant reduction in mitochondrial membrane potential in HUVECs (all P < 0.05).  Conclusion  There is a significant increase in the plasma level of EMPs in AP patients, which is correlated with the severity of pancreatitis.Meanwhile, the plasma of AP patients can promote the formation of EMPs in HUVECs in vitro, which may be associated with cell oxidative injury.

     

  • [1]
    GARG PK, SINGH VP. Organ failure due to systemic injury in acute pancreatitis[J]. Gastroenterology, 2019, 156(7): 2008-2023. DOI: 10.1053/j.gastro.2018.12.041.
    [2]
    SINGH P, GARG PK. Pathophysiological mechanisms in acute pancreatitis: Current understanding[J]. Indian J Gastroenterol, 2016, 35(3): 153-166. DOI: 10.1007/s12664-016-0647-y.
    [3]
    GE N, XIA Q, YANG ZH, et al. Vascular endothelial injury and apoptosis in rats with severe acute pancreatitis[J]. Gastroenterol Res Pract, 2015, 2015: 235017. DOI: 10.1155/2015/235017.
    [4]
    DUMNICKA P, MADUZIA D, CERANOWICZ P, et al. The interplay between inflammation, coagulation and endothelial injury in the early phase of acute pancreatitis: clinical implications[J]. Int J Mol Sci, 2017, 18(2): 354. DOI: 10.3390/ijms18020354.
    [5]
    de OLIVEIRA C, KHATUA B, NOEL P, et al. Pancreatic triglyceride lipase mediates lipotoxic systemic inflammation[J]. J Clin Invest, 2020, 130(4): 1931-1947. DOI: 10.1172/JCI132767.
    [6]
    MAHMOUD AM, WILKINSON FL, MCCARTHY EM, et al. Endothelial microparticles prevent lipid-induced endothelial damage via Akt/eNOS signaling and reduced oxidative stress[J]. FASEB J, 2017, 31(10): 4636-4648. DOI: 10.1096/fj.201601244RR.
    [7]
    PARKER B, Al-HUSAIN A, PEMBERTON P, et al. Suppression of inflammation reduces endothelial microparticles in active systemic lupus erythematosus[J]. Ann Rheum Dis, 2014, 73(6): 1144-1150. DOI: 10.1136/annrheumdis-2012-203028.
    [8]
    JALAL D, RENNER B, LASKOWSKI J, et al. Endothelial microparticles and systemic complement activation in patients with chronic kidney disease[J]. J Am Heart Assoc, 2018, 7(14): e007818. DOI: 10.1161/JAHA.117.007818.
    [9]
    ABBAS M, JESEL L, AUGER C, et al. Endothelial microparticles from acute coronary syndrome patients induce premature coronary artery endothelial cell aging and thrombogenicity: Role of the Ang Ⅱ/AT1 receptor/NADPH oxidase-mediated activation of MAPKs and PI3-kinase pathways[J]. Circulation, 2017, 135(3): 280-296. DOI: 10.1161/CIRCULATIONAHA.116.017513.
    [10]
    Al-QAISSI A, PAPAGEORGIOU M, DESHMUKH H, et al. Effects of acute insulin-induced hypoglycaemia on endothelial microparticles in adults with and without type 2 diabetes[J]. Diabetes Obes Metab, 2019, 21(3): 533-540. DOI: 10.1111/dom.13548.
    [11]
    BANKS PA, BOLLEN TL, DERVENIS C, et al. Classification of acute pancreatitis——2012: revision of the Atlanta classification and definitions by international consensus[J]. Gut, 2013, 62(1): 102-111. DOI: 10.1136/gutjnl-2012-302779.
    [12]
    POHL PH, LOZITO TP, CUPERMAN T, et al. Catabolic effects of endothelial cell-derived microparticles on disc cells: Implications in intervertebral disc neovascularization and degeneration[J]. J Orthop Res, 2016, 34(8): 1466-1474. DOI: 10.1002/jor.23298.
    [13]
    TOMKÖTTER L, ERBES J, TREPTE C, et al. The effects of pancreatic microcirculatory disturbances on histopathologic tissue damage and the outcome in severe acute pancreatitis[J]. Pancreas, 2016, 45(2): 248-253. DOI: 10.1097/MPA.0000000000000440.
    [14]
    LEROYER AS, TEDGUI A, BOULANGER CM. Role of microparticles in atherothrombosis[J]. J Intern Med, 2008, 263(5): 528-537. DOI: 10.1111/j.1365-2796.2008.01957.x.
    [15]
    PERNOMIAN L, MOREIRA JD, GOMES MS. In the view of endothelial microparticles: Novel perspectives for diagnostic and pharmacological management of cardiovascular risk during diabetes distress[J]. J Diabetes Res, 2018, 2018: 9685205. DOI: 10.1155/2018/9685205.
    [16]
    LI T, LUO N, DU L, et al. Tumor necrosis factor-α plays an initiating role in extracorporeal circulation-induced acute lung injury[J]. Lung, 2013, 191(2): 207-214. DOI: 10.1007/s00408-012-9449-x.
    [17]
    CLEMMER JS, XIANG L, LU S, et al. Hyperglycemia-mediated oxidative stress increases pulmonary vascular permeability[J]. Microcirculation, 2016, 23(3): 221-229. DOI: 10.1111/micc.12267.
    [18]
    BURGER D, TURNER M, XIAO F, et al. High glucose increases the formation and pro-oxidative activity of endothelial microparticles[J]. Diabetologia, 2017, 60(9): 1791-1800. DOI: 10.1007/s00125-017-4331-2.
    [19]
    CAO WL, XIANG XH, CHEN K, et al. Potential role of NADPH oxidase in pathogenesis of pancreatitis[J]. World J Gastrointest Pathophysiol, 2014, 5(3): 169-177. DOI: 10.4291/wjgp.v5.i3.169.
    [20]
    CHAN S, LIAN Q, CHEN MP, et al. Deferiprone inhibits iron overload-induced tissue factor bearing endothelial microparticle generation by inhibition oxidative stress induced mitochondrial injury, and apoptosis[J]. Toxicol Appl Pharmacol, 2018, 338: 148-158. DOI: 10.1016/j.taap.2017.11.005.
    [21]
    CHEN YH, CHEN ZW, LI HM, et al. AGE/RAGE-induced EMP release via the NOX-derived ROS pathway[J]. J Diabetes Res, 2018, 2018: 6823058. DOI: 10.1155/2018/6823058.
  • Relative Articles

    [1]Weiming DAI, Lungen LU, Xiaobo CAI. Association between liver sinusoidal endothelial cells and liver fibrosis[J]. Journal of Clinical Hepatology, 2023, 39(2): 419-423. doi: 10.3969/j.issn.1001-5256.2023.02.027
    [2]Yu ZHANG, Huali WANG, Shuming LU. Three cases of hepatic epithelioid hemangioendothelioma[J]. Journal of Clinical Hepatology, 2022, 38(9): 2116-2119. doi: 10.3969/j.issn.1001-5256.2022.09.031
    [3]Hao XU, Bai RUAN, Zhiwen LI, Zhiqiang FANG, Lin WANG, Kefeng DOU. Establishment of a mouse model of vascular endothelial-mesenchymal transdifferentiation genetic tracing and its role in liver fibrosis studies[J]. Journal of Clinical Hepatology, 2022, 38(4): 832-836. doi: 10.3969/j.issn.1001-5256.2022.04.018
    [4]Jin XU, Yan PENG, Chuankang TANG. Value of neutrophil-lymphocyte ratio combined with apolipoprotein A-I level in predicting the severity of acute pancreatitis in the early stage after admission[J]. Journal of Clinical Hepatology, 2021, 37(3): 660-665. doi: 10.3969/j.issn.1001-5256.2021.03.030
    [5]Wei BiWei, Gong YaHui, Liang ZhiHai. Role of pyroptosis in the pathogenesis of acute pancreatitis[J]. Journal of Clinical Hepatology, 2020, 36(8): 1905-1908. doi: 10.3969/j.issn.1001-5256.2020.08.050
    [6]Qi QinQin, Yang Bin, Li HuiHui, Bao JunJun, Li HongYe, Wang BingBing, Mei Qiao. Level of platelet microparticles in acute pancreatitis and their role in the formation of neutrophil extracellular traps[J]. Journal of Clinical Hepatology, 2020, 36(4): 870-873. doi: 10.3969/j.issn.1001-5256.2020.04.032
    [7]Jiang Zhao, Ruan Bo. The role of liver sinusoidal endothelial cells in the progression of nonalcoholic fatty liver disease[J]. Journal of Clinical Hepatology, 2020, 36(3): 684-686. doi: 10.3969/j.issn.1001-5256.2020.03.047
    [8]Zhu ZiYi, Liu Yuan, Wang WenBo, Jiang ZhongYong, Chang Kai, Ye YuSheng, Xiong Jie. Mechanism of HCV stimulation of human umbilical vein endothelial cells in the pathogenesis of atherosclerosis[J]. Journal of Clinical Hepatology, 2019, 35(6): 1313-1317. doi: 10.3969/j.issn.1001-5256.2019.06.026
    [9]Yu ZiYue, Lin Xin, Han Ying, Cui LiNa. Role of liver sinusoidal endothelial cells in liver regeneration and the development of liver fibrosis[J]. Journal of Clinical Hepatology, 2019, 35(9): 2072-2074. doi: 10.3969/j.issn.1001-5256.2019.09.041
    [10]Wang Lin, Liu XueEn, Zhuang Hui. Cellular mechanisms in liver fibrosis regression[J]. Journal of Clinical Hepatology, 2018, 34(4): 862-866. doi: 10.3969/j.issn.1001-5256.2018.04.036
    [11]Zhu ZeMin, Xie ZhiQin, Zhao ZhiJian, Li HongXia, Xu Tao, Tang CaiXi. Pancreatic acinar cell carcinoma with acute pancreatitis as the first symptom: A case report[J]. Journal of Clinical Hepatology, 2018, 34(12): 2662-2664. doi: 10.3969/j.issn.1001-5256.2018.12.032
    [12]Hu QingMei, Niu ChunYan. Predictive value of combined measurement of D-dimer, fibrinogen, and peripheral blood leukocyte count for severity of acute pancreatitis[J]. Journal of Clinical Hepatology, 2017, 33(8): 1522-1526. doi: 10.3969/j.issn.1001-5256.2017.08.023
    [13]Wang Yan, Cui LiJian, Xiao HongLi, Wang GuoXing, Yin ChengHong. Effect of angiotensin 1-7 on the TLR4/NF-κB pathway in cerulein-induced pancreatic acinar cells[J]. Journal of Clinical Hepatology, 2016, 32(11): 2146-2150. doi: 10.3969/j.issn.1001-5256.2016.11.029
    [14]Jiao ShuHua, Liu PengLiang, Wen YanHui. Combined determination of serum C-reactive protein,lipase,interleukin-1β,and intercellular adhesion molecule1 in early identification of severity of acute pancreatitis[J]. Journal of Clinical Hepatology, 2016, 32(1): 131-134. doi: 10.3969/j.issn.1001-5256.2016.01.025
    [15]Hao TingTing, Ma XiaoPeng, Wen YanLi, Dai GuangRong, Feng YiChao, Zhang Li. Changes in serum levels of M30,M65,and IL-17 and their clinical significance in patients with acute pancreatitis[J]. Journal of Clinical Hepatology, 2016, 32(2): 329-332. doi: 10.3969/j.issn.1001-5256.2016.02.027
    [16]Lu Wang, Zhang Rui, Jiang HongLi, Hu YuLin, Xin GuiJie. One case of hepatic epithelioid hemangioendothelioma[J]. Journal of Clinical Hepatology, 2015, 31(8): 1330-1331. doi: 10.3969/j.issn.1001-5256.2015.08.038
    [17]Wu Gang, Zheng Jie, Hu GuoXin, Peng YanZhong. Role of liver nonparenchymal cells in hepatic ischemia-reperfusion injury[J]. Journal of Clinical Hepatology, 2014, 30(12): 1366-1369. doi: 10.3969/j.issn.1001-5256.2014.12.033
    [18]Ren LiNan, Guo XiaoZhong, Zou DeLi. EG-VEGF expression and significance in pancreatic carcinoma[J]. Journal of Clinical Hepatology, 2012, 28(8): 589-591.
  • Cited by

    Periodical cited type(15)

    1. 许娟,闫涛涛,李严锋,侯静涛,樊研. ALBI评分联合PCT在肝硬化腹水患者自发性细菌性腹膜炎的预测作用. 胃肠病学和肝病学杂志. 2023(01): 85-89 .
    2. 周苏云,周影,程新月. 肝硬化患者发生肝性脑病的影响因素分析及对预检分诊意义的探讨. 中西医结合护理(中英文). 2023(03): 130-132 .
    3. 方翊天,吴若林,黄帆,王国斌,冯丽娟,余孝俊,侯刘进,叶征辉,耿小平,赵红川. 肝移植术后多重耐药菌感染危险因素的单中心临床研究. 器官移植. 2021(02): 197-202 .
    4. 李尚书,刘群,黄丽雯. 慢性肝病血小板减少的原因. 中国肝脏病杂志(电子版). 2021(02): 24-28 .
    5. 陆素芳,周红,王丹丹,陈益群,赵红利,张勇杨. MELD评分联合SII对失代偿期肝硬化患者预后的预测作用. 现代消化及介入诊疗. 2021(08): 973-977 .
    6. 黄敏,李冬冬,刘传苗. 乙肝相关慢加急性肝衰竭患者临床短期预后因素的分析. 中华全科医学. 2021(12): 2028-2030 .
    7. 贾亚男,李瀚,李先亮,贺强. 危重症肝病肝移植患者诊断和评估标准的临床进展. 器官移植. 2020(03): 326-331+368 .
    8. 姚运海,赵卫峰,甘建和. 苏州地区血吸虫性肝病患者临床特征及外周血T淋巴细胞亚群分布. 中国血吸虫病防治杂志. 2020(02): 154-158+167 .
    9. 张耀弟. △CTP评分评估肝硬化患者短期预后的价值分析. 甘肃科技. 2020(09): 117-118+152 .
    10. 刘小婷,杨欢,姚红,任小婵,罗选娟,王小闯. 碳青霉烯类耐药肺炎克雷伯菌感染死亡风险预测模型的建立及其对患者预后的预测价值研究. 中国全科医学. 2020(30): 3789-3797 .
    11. 韩志钧,韩柠泽,闫伟,马金彤. 肝血流动力学变化与肝储备功能相关性的研究. 中华医学超声杂志(电子版). 2020(06): 563-565 .
    12. 寇建涛,刘喆,朱继巧,马军,许文犁,李瀚,贾亚男,李先亮,贺强. 肝移植治疗危重症肝病的临床疗效研究. 器官移植. 2020(04): 482-486 .
    13. 宋梅,汪明星,李乐,何进伟,何丽丽. MELD评分结合降钙素原评估终末期肝病预后的临床分析. 中国医药科学. 2020(09): 254-256 .
    14. 李帆,成金英,刘贤贤,丁国锋. 乙肝肝硬化并发甲型流感及肺曲霉菌病1例并文献复习. 中国当代医药. 2020(34): 214-217 .
    15. 韩志钧,韩柠泽,闫伟,马金彤. 肝血流动力学变化与吲哚菁绿代谢试验评价肝储备功能的对比. 医学研究与教育. 2019(06): 28-31 .

    Other cited types(1)

  • 加载中
    Created with Highcharts 5.0.7Chart context menuAccess Class DistributionFULLTEXT: 24.8 %FULLTEXT: 24.8 %META: 69.6 %META: 69.6 %PDF: 5.5 %PDF: 5.5 %FULLTEXTMETAPDF

Catalog

    通讯作者: 陈斌, bchen63@163.com
    • 1. 

      沈阳化工大学材料科学与工程学院 沈阳 110142

    1. 本站搜索
    2. 百度学术搜索
    3. 万方数据库搜索
    4. CNKI搜索

    Figures(4)  / Tables(2)

    Article Metrics

    Article views (429) PDF downloads(34) Cited by(16)
    Proportional views
    Related

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return