切换至 "中华医学电子期刊资源库"

中华危重症医学杂志(电子版) ›› 2020, Vol. 13 ›› Issue (06) : 401 -405. doi: 10.3877/cma.j.issn.1674-6880.2020.06.001

所属专题: 文献

论著

自噬蛋白Beclin1及炎症因子表达在脓毒症急性肾损伤中的作用
刘颖1, 孟超1, 赵谊1, 邹磊1, 李晨辉1, 付润1, 刘汉1,()   
  1. 1. 210006 南京,南京医科大学附属南京医院(南京市第一医院)重症医学科
  • 收稿日期:2020-03-17 出版日期:2020-12-31
  • 通信作者: 刘汉
  • 基金资助:
    南京市医学科技发展项目(YKK16123)

Role of autophagy protein Beclin1 and inflammatory factors in sepsis with acute kidney injury

Ying Liu1, Chao Meng1, Yi Zhao1, Lei Zou1, Chenhui Li1, Run Fu1, Han Liu1,()   

  1. 1. Department of Critical Care Medicine, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, China
  • Received:2020-03-17 Published:2020-12-31
  • Corresponding author: Han Liu
引用本文:

刘颖, 孟超, 赵谊, 邹磊, 李晨辉, 付润, 刘汉. 自噬蛋白Beclin1及炎症因子表达在脓毒症急性肾损伤中的作用[J/OL]. 中华危重症医学杂志(电子版), 2020, 13(06): 401-405.

Ying Liu, Chao Meng, Yi Zhao, Lei Zou, Chenhui Li, Run Fu, Han Liu. Role of autophagy protein Beclin1 and inflammatory factors in sepsis with acute kidney injury[J/OL]. Chinese Journal of Critical Care Medicine(Electronic Edition), 2020, 13(06): 401-405.

目的

探讨自噬蛋白Beclin1及炎症因子表达在脓毒症急性肾损伤(AKI)中的作用。

方法

选择2017年1月至2019年6月南京医科大学附属南京医院ICU收治的86例脓毒症患者,根据患者入ICU时是否合并AKI,将86例患者分成AKI组(33例)和非AKI组(53例)。记录所有患者入ICU时血清胱抑素C、肿瘤坏死因子、干扰素、白细胞介素6(IL-6)、IL-10以及入ICU时和第7天外周静脉血自噬蛋白Beclin1及P62的表达水平。采用Pearson相关分析脓毒症患者自噬蛋白Beclin1与胱抑素C、IL-6的相关性。

结果

AKI组脓毒症患者入ICU时和第7天Beclin1蛋白水平均较同时间点非AKI组显著升高(t = 5.213、7.144,P = 0.007、0.002),P62蛋白水平均较同时间点非AKI组显著降低(t = 4.618、7.223,P = 0.025、0.003);AKI组患者第7天Beclin1蛋白水平较入ICU时显著升高(t = 4.865,P = 0.006),而P62蛋白水平较入ICU时显著降低(t = 5.996,P = 0.006)。AKI组患者入ICU时血清胱抑素C [(2.4 ± 0.5)mg / L vs.(1.3 ± 0.4)mg / L]及IL-6 [(613 ± 163)ng / L vs.(269 ± 124)ng / L]表达水平均显著高于非AKI组患者(t = 10.459、11.068,P均< 0.001)。Pearson相关分析结果显示,脓毒症患者自噬蛋白Beclin1表达水平与血清胱抑素C(r = 0.949,P = 0.001)、IL-6(r = 0.824,P = 0.012)均呈正相关。

结论

脓毒症患者发生AKI与自噬蛋白Beclin1及炎症因子异常表达有关。

Objective

To investigate the role of autophagy protein Beclin1 and inflammatory factors in patients with sepsis and acute kidney injury (AKI).

Methods

A total of 86 patients with sepsis admitted to the ICU of Nanjing First Hospital, Nanjing Medical University from January 2017 to June 2019 were divided into an AKI group (n = 33) and a non-AKI group (n = 53) according to whether they were combined with AKI at ICU admission. The serum cystatin C, tumor necrosis factor, interferon, interleukin-6 (IL-6) and IL-10 at ICU admission and the expression levels of autophagy protein Beclin1 and P62 in peripheral venous blood at the time of ICU admission and 7th day were recorded for all patients. Pearson correlation was used to analyze the correlation of Beclin1 with cystatin C and IL-6 in septic patients.

Results

The Beclin1 protein levels were significantly higher (t = 5.213, 7.144; P = 0.007, 0.002) and the P62 protein levels were significantly lower (t = 4.618, 7.223; P = 0.025, 0.003) in the AKI group than in the non-AKI group both at the time of ICU admission and 7th day. In the AKI group, the Beclin1 protein level was significantly higher (t = 4.865, P = 0.006) and the P62 protein level was significantly lower (t = 5.996, P = 0.006) at the 7th day than at ICU admission. The expression levels of cystatin C [(2.4 ± 0.5) mg / L vs. (1.3 ± 0.4) mg / L] and IL-6 [(613 ± 163) ng / L vs. (269 ± 124) ng / L] were significantly higher in the AKI group than in the non-AKI group at ICU admission (t = 10.459, 11.068; both P < 0.001). Pearson correlation analysis showed that the Beclin1 level of patients with sepsis was positively correlated with cystatin C (r = 0.949, P = 0.001) and IL-6 (r = 0.824, P = 0.012).

Conclusion

The occurrence of AKI in patients with sepsis is associated with abnormal expression levels of autophagy protein Beclin1 and inflammatory factors.

图1 脓毒症AKI与非AKI患者血Beclin1及P62蛋白表达水平的比较
表1 两组脓毒症患者入ICU时血清胱抑素C与炎症因子含量的比较(±s
9
Legrand M, Bezemer R, Kandil A, et al. The role of renal hypoperfusion in development of renal microcirculatory dysfunction in endotoxemic rats[J]. Intensive Care Med, 2011, 37 (9): 1534-1542.
10
Bagshaw SM, Lapinsky S, Dial S, et al. Acute kidney injury in septic shock: clinical outcomes and impact of duration of hypotension prior to initiation of antimicrobial therapy[J]. Intensive Care Med, 2009, 35 (5): 871-881.
11
Kellum JA, Prowle JR. Paradigms of acute kidney injury in the intensive care setting[J]. Nat Rev Nephrol, 2018, 14 (4): 217-230.
12
He L, Livingston MJ, Dong Z. Autophagy in acute kidney injury and repair[J]. Nephron Clin Pract, 2014, 127 (1-4): 56-60.
13
Su Y, Qu Y, Zhao F, et al. Regulation of autophagy by the nuclear factor κB signaling pathway in the hippocampus of rats with sepsis[J]. J Neuroinflammation, 2015 (12): 116.
14
Jones SA, Mills KH, Harris J. Autophagy and infl-ammatory diseases[J]. Immunol Cell Biol, 2013, 91 (3): 250-258.
15
Sinha S, Levine B. The autophagy effector Beclin 1: a novel BH3-only protein[J]. Oncogene, 2008, 27 (Suppl 1): S137-S148.
16
Lamark T, Svenning S, Johansen T. Regulation of se-lective autophagy: the p62 / SQSTM1 paradigm[J]. Essays Biochem, 2017, 61 (6): 609-624.
17
Kellum JA, Lameire N, KDIGO AKI Guideline Work Group. Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1)[J]. Crit Care, 2013, 17 (1): 204.
18
Angeli P, Ginès P, Wong F, et al. Diagnosis and m-anagement of acute kidney injury in patients with cirrhosis: revised consensus recommendations of the International Club of Ascites[J]. Gut, 2015, 64 (4): 531-537.
19
Linder A, Fjell C, Levin A, et al. Small acute inc-reases in serum creatinine are associated with decreased long-term survival in the critically ill[J]. Am J Respir Crit Care Med, 2014, 189 (9): 1075-1081.
20
Liu XJ, Hong Q, Wang Z, et al. MicroRNA-34a su-ppresses autophagy in tubular epithelial cells in acute kidney injury[J]. Am J Nephrol, 2015, 42 (2): 168-175.
21
Liu H, Gu LB, Tu Y, et al. Emodin ameliorates ci-splatin-induced apoptosis of rat renal tubular cells in vitro by activating autophagy[J]. Acta Pharmacol Sin, 2016, 37 (2): 235-245.
22
Lerolle N, Nochy D, Guérot E, et al. Histopathology of septic shock induced acute kidney injury: apoptosis and leukocytic infiltration[J]. Intensive Care Med, 2010, 36 (3): 471-478.
23
Jacobs R, Honore PM, Joannes-Boyau O, et al. Septic acute kidney injury: the culprit is inflammatory apoptosis rather than ischemic necrosis[J]. Blood Purif, 2011, 32 (4): 262-265.
24
郑丽云,薛群,倪健强,等. 多发性硬化和视神经脊髓炎患者外周血单个核细胞中Beclin1与LC3的表达及其意义[J]. 中华医学杂志,2014,94(39):3052-3055.
25
Onopiuk A, Tokarzewicz A, Gorodkiewicz E. Cystatin C: a kidney function biomarker[J]. Adv Clin Chem, 2015 (68): 57-69.
26
赵健斌,谭宁,刘勇,等. 术前胱抑素C水平对冠脉介入术后急性肾损伤发生和远期不良预后的预测价值[J]. 实用医学杂志,2016,32(8):1254-1257.
27
Ortuno-Andériz F, Cabello-Clotet N, Vidart-Simón N, et al. Cystatin C as an early marker of acute kidney injury in septic shock[J]. Rev Clin Esp, 2015, 215 (2): 83-90.
1
Rhodes A, Evans LE, Alhazzani W, et al. Surviving Sepsis Campaign: international guidelines for management of sepsis and septic shock: 2016[J]. Crit Care Med, 2017, 43 (3): 486-552.
2
Perner A, Cecconi M, Cronhjort M, et al. Expert sta-tement for the management of hypovolemia in sepsis[J]. Intensive Care Med, 2018, 44 (6): 791-798.
3
Guo C, Dong G, Liang X, et al. Epigenetic regulation in AKI and kidney repair: mechanisms and therapeutic implications[J]. Nat Rev Nephrol, 2019, 15 (4): 220-239.
4
Reinhart K, Daniels R, Kissoon N, et al. Recognizing sepsis as a Global Health Priority-a WHO resolution[J]. N Engl J Med, 2017, 377 (5): 414-417.
5
Gómez H, Kellum JA. Sepsis-induced acute kidney in-jury[J]. Curr Opin Crit Care, 2016, 22 (6): 546-553.
6
Zafrani L, Ergin B, Kapucu A, et al. Blood transfusion improves renal oxygenation and renal function in sepsis-induced acute kidney injury in rats[J]. Crit Care, 2016, 20 (1): 406.
7
Castoldi A, Braga TT, Correa-Costa M, et al. TLR2, TLR4 and the MYD88 signaling pathway are crucial for neutrophil migration in acute kidney injury induced by sepsis[J]. PLoS One, 2012, 7 (5): e37584.
8
Zarjou A, Agarwal A. Sepsis and acute kidney injury[J]. J Am Soc Nephrol, 2011, 22 (6): 999-1006.
[1] 吴杰, 周志强, 符菁, 李喜功, 张钦. 吸入性氢气对大鼠脊髓损伤后自噬及神经功能的影响[J/OL]. 中华危重症医学杂志(电子版), 2024, 17(05): 363-371.
[2] 庄燕, 戴林峰, 张海东, 陈秋华, 聂清芳. 脓毒症患者早期生存影响因素及Cox 风险预测模型构建[J/OL]. 中华危重症医学杂志(电子版), 2024, 17(05): 372-378.
[3] 李争光, 宰爽嘉, 吴火峰, 孙华, 张永博, 陈浏阳, 戴睿, 张亮. 昼夜节律相关因子在椎间盘退行性变发病机制中作用的研究进展[J/OL]. 中华损伤与修复杂志(电子版), 2024, 19(05): 457-461.
[4] 杜贵伟, 陆勇, 成博, 贺薏, 梁爽. 钬激光碎石术术后联合坦索罗辛治疗对输尿管结石患者的影响分析[J/OL]. 中华腔镜泌尿外科杂志(电子版), 2024, 18(05): 491-496.
[5] 高娟, 徐建庆, 闫芳, 丁盛华, 刘霞. Rutkow、TAPP、TEP 手术治疗单侧腹股沟疝患者的临床疗效及对血清炎症因子水平的影响[J/OL]. 中华疝和腹壁外科杂志(电子版), 2024, 18(06): 675-680.
[6] 邢嘉翌, 龚佳晟, 祝佳佳, 陆群. 肺癌化疗患者继发肺部感染的病原菌耐药性及炎症因子变化分析[J/OL]. 中华肺部疾病杂志(电子版), 2024, 17(05): 714-718.
[7] 杜霞, 马梦青, 曹长春. 造影剂诱导的急性肾损伤的发病机制及干预靶点研究进展[J/OL]. 中华肾病研究电子杂志, 2024, 13(05): 279-282.
[8] 郭俊楠, 林惠, 任艺林, 乔晞. 氨基酸代谢异常在急性肾损伤向慢性肾脏病转变中的作用研究进展[J/OL]. 中华肾病研究电子杂志, 2024, 13(05): 283-287.
[9] 司楠, 孙洪涛. 创伤性脑损伤后肾功能障碍危险因素的研究进展[J/OL]. 中华脑科疾病与康复杂志(电子版), 2024, 14(05): 300-305.
[10] 史清泉, 苗彬, 王烁, 陶琳, 沈晨. miR-181a-5p 靶向ATG5 抑制雨蛙素诱导的大鼠胰腺腺泡细胞AR42J自噬的机制研究[J/OL]. 中华消化病与影像杂志(电子版), 2024, 14(06): 524-530.
[11] 沈炎, 张俊峰, 唐春芳. 预后营养指数结合血清降钙素原、胱抑素C及视黄醇结合蛋白对急性胰腺炎并发急性肾损伤的预测价值[J/OL]. 中华消化病与影像杂志(电子版), 2024, 14(06): 536-540.
[12] 陈惠英, 邱敏珊, 邵汉权. 脓毒症诱发肠黏膜屏障功能损伤的风险因素模型构建与应用效果[J/OL]. 中华消化病与影像杂志(电子版), 2024, 14(05): 448-452.
[13] 颜世锐, 熊辉. 感染性心内膜炎合并急性肾损伤患者的危险因素探索及死亡风险预测[J/OL]. 中华临床医师杂志(电子版), 2024, 18(07): 618-624.
[14] 欧春影, 李晓宾, 郭靖, 朱亮, 许可, 王梦, 安晓雷. 丁苯酞对血管性认知障碍大鼠炎症因子的影响及对认知障碍的改善作用[J/OL]. 中华脑血管病杂志(电子版), 2024, 18(05): 483-487.
[15] 牟磊, 徐东成, 韩鑫, 徐长江, 韩坤锜, 薛叶潇, 牟媛, 秦文玲, 刘相静, 陈哲, 高楠. 五虫通络胶囊防治椎动脉开口支架术后再狭窄发生的效果[J/OL]. 中华脑血管病杂志(电子版), 2024, 18(05): 467-472.
阅读次数
全文


摘要


AI


AI小编
你好!我是《中华医学电子期刊资源库》AI小编,有什么可以帮您的吗?