|本期目录/Table of Contents|

[1]甘丽杏,郑永超.阿奇霉素对COPD急性发作期患者组蛋白去乙酰化酶2表达影响[J].中华肺部疾病杂志,2021,(03):321-324.[doi:10.3877/cma.j.issn.1674-6902.2021.03.014]
点击复制

阿奇霉素对COPD急性发作期患者组蛋白去乙酰化酶2表达影响(PDF)

《中华肺部疾病杂志》[ISSN:1006-6977/CN:61-1281/TN]

卷:
期数:
2021年03期
页码:
321-324
栏目:
临床研究
出版日期:
2021-06-20

文章信息/Info

Title:
-
作者:
甘丽杏1; 郑永超2
200011 上海,上海交通大学医学院附属第九人民医院呼吸与危重症医学科1 麻醉科2
Author(s):
-
关键词:
肺疾病; 慢性阻塞性;  肿瘤坏死因子-α;  白介素-8;  组蛋白去乙酰化酶2;  阿奇霉素;  糖皮质激素抵抗
Keywords:
-
分类号:
-
DOI:
10.3877/cma.j.issn.1674-6902.2021.03.014
摘要:
目的 探讨慢性阻塞性肺疾病(COPD)患者在急性发作期血液中白介素-8(IL-8)、肿瘤坏死因子(TNF-α)以及组蛋白去乙酰化酶2(HDAC2)表达。观察阿奇霉素、地塞米松等药物体外干预对COPD急性发作期(AECOPD)血液中炎症因子以及HDAC2表达影响。方法 COPD稳定期患者13例为对照组,抽取空腹静脉血5 ml。AECOPD组患者15例,分别抽取空腹静脉血20 ml+5 ml,静脉血分别取上清后提取单个核细胞,酶联免疫吸附法(ELISA)检测上清中IL-8和TNF-α表达; Western blot方法检测两组单核细胞中HDAC2表达。15例AECOPD患者20 ml静脉血提取单核细胞重悬后分成阿奇霉素、地塞米松、阿奇霉素联合地塞米松共培养24 h,取上清,收集单核细胞。ELISA检测上清中IL-8和TNF-α表达; Western blot方法检测单核细胞中HDAC2表达。 结果 AECOPD组炎症因子的表达较对照组明显升高,IL-8[(210.23±18.83)pg/ml vs.(98.97±11.13)pg/ml(P<0.01)]、TNF-α[(130.17±16.78)pg/ml vs.(67.47±8.07)pg/ml(P<0.01)]。AECOPD组、阿奇霉素培养组、地塞米松培养组、阿奇霉素+地塞米松共培养分组,IL-8表达分别为(82.60±6.47)pg/ml,(76.58±5.72)pg/ml,(77.01±5.13)pg/ml,(66.88±5.42)pg/ml; TNF-α的表达分别为(52.55±9.04)pg/ml,(46.50±6.44)pg/ml,(45.64±6.66)pg/ml,(41.70±5.57)pg/ml; 阿奇霉素、地塞米松均能降低炎症因子表达,而阿奇霉素+地塞米松共培养组炎症因子表达较单用地塞米松组降低(P<0.05)。AECOPD组HDAC2表达较对照组降低[(1.18±0.16)vs.(1.27±0.21)(P<0.05)]。AECOPD外周血单核细胞按照AECOPD组、阿奇霉素培养组、地塞米松培养组、阿奇霉素+地塞米松共培养组分组,HDAC2表达分别为(0.66±0.22)、(0.73±0.24)、(0.90±0.15)、(1.15±0.12),地塞米松能部分恢复HDAC2表达(P<0.05); 阿奇霉素+地塞米松共培养组较单用地塞米松组能更好的恢复HDAC2表达(P<0.01)。结论 对照组,AECOPD组患者IL-8、TNF-α表达升高,地塞米松与阿奇霉素均能降低炎症因子表达。
Abstract:
-

参考文献/References:

1 任成山, 王关嵩, 钱桂生. 慢性阻塞性肺疾病的成因及其治疗的困惑与希望[J/CD]. 中华肺部疾病杂志(电子版), 2019, 12(2): 127-141.
2 Mei D, Tan WSD, Wong WSF. Pharmacological strategies to regain steroid sensitivity in severe asthma and COPD[J]. Curr Opin Pharmacol. 2019, 46: 73-81.
3 Meja KK, Rajendrasozhan S, Adenuga D, et al. Curcumin restores corticosteroid function in monocytes exposed to oxidants by maintaining HDAC2[J]. Am J Respir Cell Mol Biol, 2008, 39(3): 312-323.
4 Barnes PJ. Role of HDAC2 in the pathophysiology of COPD[J]. Annu Rev Physiol, 2009, 71: 451-464.
5 Gan LX, Li CY, Guo XJ, et al. Curcumin modulates the effect of histone modification on the expression of chemokines by type Ⅱ alveolar epithelial cells in a rat COPD model[J]. Int J Chron Obstruct Pulmon Dis, 2016, 11: 2765-2773.
6 甘丽杏, 李成业, 郭雪君. 慢性阻塞性肺疾病组蛋白去乙酰化酶与糖皮质激素抵抗[J]. 国际呼吸杂志, 2010, 30(5): 283-285.
7 Tamimi A, Serdarevic D, Hanania NA. The effects of cigarette smoke on airway inflammation in asthma and COPD: therapeutic implications[J]. Respir Med, 2012, 106(3): 319-328.
8 Cheng SE, Luo SF, Jou MJ, et al. Cigarette smoke extract induces cytosolic phospholipase A2 expression via NADPH oxidase, MAPKs, AP-1, and NF-kappaB in human tracheal smooth muscle cells[J]. Free Radic Biol Med, 2009, 46(7): 948-960.
9 Adcock IM, Tsaprouni L, Bhavsar P, et al. Epigenetic regulation of airway inflammation[J]. Curr Opin Immunol, 2007, 19(6): 694-700.
10 Spagnolo P, Fabbri LM, Bush A. Long-term macrolide treatment for chronic respiratory disease[J]. Eur Respir J, 2013, 42(1): 239-251.
11 Sun XJ, Chen L, He ZY. PI3K/Akt-Nrf2 and anti-inflammation effect of macrolides in chronic obstructive pulmonary disease[J]. Current Drug Metabolism, 2019, 20, 301-304.
12 Cao YQ, Xuan SR, Wu YH. Effects of long-term macrolide therapy at low doses in stable COPD[J]. Int J Chron Obstruct Pulmon Dis, 2019, 14: 1289-1298.
13 Tadeusz Pusa. Azithromycin in the treatment of patients with exacerbation of chronic obstructive pulmonary disease[J]. Pol Merkur Lekarski, 2020, 48(283): 65-68.
14 Qiu SL, Zhong XN. Macrolides: a promising pharmacologic therapy for chronic obstructive pulmonary disease[J]. Ther Adv Respir Dis, 2017, 11(3): 147-155.
15 中华医学会呼吸病学慢性阻塞性肺疾病组. 慢性阻塞性肺疾病诊治指南(2007年修订版)[J]. 中华内科杂志, 2007, 46(43): 254-261.
16 慢性阻塞性肺疾病急性加重(AECOPD)诊治专家组[J]. 国际呼吸杂志, 2017, 37(14): 1041-1057.
17 Seemungal TA, Harper-owen R, Bhowmik A, et al. Detection of rhinovirus in induced sputum at exacerbation of chronic obstructive pulmonary disease[J]. Eur Respir J, 2000, 16(4): 677-683.
18 杨 阳, 杨 雁. COPD缓解期患者血清PCT、IL-6、hs-CRP水平对急性加重的预测作用[J]. 广东医学, 2017, 38(10): 1531-1533.
19 Barnes PJ. Glucocorticoid resistance in patients with asthma and chronic obstructive pulmonary disease [J]. Allergy Clin. Immunol, 2013, 3(131): 636-645.
20 王 飞, 贺 蓓. 组蛋白去乙酰化酶在慢性阻塞性肺疾病中的重要作用[J]. 国际呼吸杂志, 2007, 27(13): 985-988.
21 Jiang ZL, Zhu L. Update on molecular mechanisms of corticosteroid resistance in chronic obstructive pulmonary disease[J]. Pulm Pharmacol Ther, 2016, 37: 1-8.
22 Ito K, Chung KF, Adcock IM. Update on glucocorticoid action and resistance[J]. Allergy Clin Immunol, 2006, 117: 522-543.
23 甘丽杏, 熊维宁, 郭雪君. 慢性阻塞性肺疾病炎症因子与组蛋白去乙酰化酶2表达的临床意义[J/CD]. 中华肺部疾病杂志, 2021, 14(2): 195-198.
24 Hull EE, Montgomery MR, Leyva KJ. HDAC2 inhibitors as epigenetic regulators of the immune system: impacts on cancer therapy and inflammatory diseases[J]. Biomed Res Int, 2016, 2016: 8797206.
25 Joseph F, Patrick M, Andrew LD, et al. Oxidative and nitrosative stress and histone deacetylase-2 activity in exacerbations of chronic obstructive pulmonary disease[J]. Chest, 2016, 149(1): 62-73.
26 Parnham MJ, Erakovic HV, Giamarellosbourboulis EJ, et al. Azithromycin: mechanisms of action and their relevance for clinical applications[J]. Pharmacol Ther, 2014, 143(2): 225-245.
27 姚志刚, 吴艳军, 谭春婷, 等. 阿奇霉素对香烟烟雾凝集物刺激的巨噬细胞炎症调控的机制研究[J]. 临床和实验医学杂志, 2019, 18(23): 2465-2468.
28 Pusa T. Azithromycin in the treatment of patients with exacerbation of chronic obstructive pulmonary disease[J]. Pol Merkur Lekarski, 2020, 48(283): 65-68.

备注/Memo

备注/Memo:
基金项目: 上海高校青年教师培养资助计划(ZZjdyx13101)
通信作者: 郑永超, Email: yongchao0110@163.com
更新日期/Last Update: 2021-06-20