不同光照方式对重症AECOPD患者血清褪黑素及氧化应激水平的影响

盖美华; 富燕萍; 金艾香; 姚惠萍

doi:10.16766/j.cnki.issn.1674-4152.002673

不同光照方式对重症AECOPD患者血清褪黑素及氧化应激水平的影响

doi: 10.16766/j.cnki.issn.1674-4152.002673

1.
浙江省人民医院/杭州医学院附属人民医院头颈甲状腺外科，浙江杭州 3100141
2.
浙江省人民医院/杭州医学院附属人民医院重症医学科

基金项目:

浙江省医药卫生科技计划项目 2020KY444

详细信息

通讯作者:
姚惠萍, E-mail: 1390906298@qq.com

中图分类号: R563
计量
- 文章访问数: 204
- HTML全文浏览量: 169
- PDF下载量: 8
- 被引次数: 0
出版历程
- 收稿日期: 2021-08-16
- 网络出版日期: 2022-11-30

Influence on levels of melatonin and oxidative stress in critically ill patients with AECOPD treated by different ways of light

1.
Department of Head and Neck Thyroid Surgery, Zhejiang Provincial People ' s Hospital/People's Hospital Affiliated Hangzhou Medical College, Hangzhou, Zhejiang 310014, China

摘要

摘要: 目的探讨不同光照方式对重症慢性阻塞性肺疾病急性加重期(AECOPD)患者血清褪黑素(Mel)及氧化应激水平的影响。方法选取浙江省人民医院ICU 2019年7月—2020年12月收治的100例AECOPD患者为研究对象，按照随机数字表法分为对照组(48例)和观察组(52例)。对照组给予24 h不间断光照，观察组采用间断光照方式。检测2组血清Mel、尿6-磺酸基褪黑素(6-SMT)、肺泡灌洗液(BALF)中丙二醛(MDA)及超氧化物歧化酶(SOD)水平并进行统计学分析。结果观察组和对照组血清Mel(早上7点及晚上10点)在入院后第5天分别为(29.6±5.8)pg/mL、(26.7±6.4)pg/mL和(50.8±8.5)pg/mL、(46.7±9.1)pg/mL，入院后第10天分别为(35.3±8.2)pg/mL、(24.5±5.7)pg/mL和(55.6±6.6)pg/mL、(44.5±7.5)pg/mL。与对照组相比，观察组血清Mel(早上7点及晚上10点)水平均呈现出逐渐升高趋势(均P＜0.05)。2组尿6-SMT(早上7点及晚上10点)水平也呈现出相似趋势。观察组BALF中MDA水平逐渐下降而SOD水平逐渐升高(均P＜0.05)。与对照组相比观察组撤机成功率明显升高，而ICU停留时间、MODS发生率和28天病死率均明显降低(均P＜0.05)。结论对重症AECOPD患者实施间断光照能够明显提高患者体内褪黑素及其代谢产物水平，提高抗氧化应激能力，改善预后。
- 慢性阻塞性肺疾病急性加重期 /
- 光照方式 /
- 褪黑素 /
- 氧化应激
Abstract: Objective To discuss the influence on levels of melatonin (Mel) and oxidative stress in critically ill patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) treated by different ways of light. Methods One hundred patients with AECOPD admitted to the Intensive Care Unit (ICU) of Zhejiang Province People ' s Hospital from July 2019 to December 2020 were selected as study subjects and divided into the control group (n=48) and observation group (n=52) according to random number table. The patients of control group were given 24-hour illumination, while the patients of observation group were given intermittent light way. The levels of serum Mel and urine 6-sulfonic melatonin (6-SMT), malondialdehyde (MDA) and superoxide dismutase (SOD) in bronchoalveolar lavage fluid (BALF) were measured, and statistical analysis were carried out. Results The levels of serum Mel (7 a.m. and 10 p.m.) were (29.6±5.8) pg/mL, (26.7±6.4) pg/mL and (50.8±8.5) pg/mL, (46.7±9.1) pg/mL respectively at 5 days after admission. The levels of serum Mel (7 a.m. and 10 p.m.) were (35.3±8.2) pg/mL, (24.5±5.7) pg/mL and (55.6±6.6) pg/mL, (44.5±7.5) pg/mL respectively at 10 days after admission. Compared with the control group, the levels of serum Mel (7 a.m. and 10 p.m.) in the observation group showed a gradually increasing trend (all P < 0.05). The levels of urine 6-SMT (7 a.m. and 10 p.m.) in the two groups showed a similar trend. In the observation group, the level of MDA in BALF gradually decreased while the level of SOD gradually increased (all P < 0.05). The success rate of removing ventilator of the observation group was obviously higher than that of the control group, while ICU stay time, the incidence of MODS and 28-day mortality were lower than those of the control group (all P < 0.05). Conclusion For critically ill patients with AECOPD, intermittent illumination can obviously increase the level of melatonin and its metabolites in the body, improve the ability of resistance to oxidative stress and improve prognosis.
- Acute exacerbation of chronic obstructive pulmonary disease /
- Light way /
- Melatonin /
- Oxidative stress

HTML全文

表 1 2组AECOPD患者一般临床资料比较

Table 1. Comparison of general clinical data between two groups of patients with AECOPD

项目	对照组(n=48)	观察组(n=52)	统计量	P值
年龄(x±s，岁)	59.2±7.4	59.5±6.2	0.220^a	0.826
性别[例(%)]			0.019^b	0.899
男性	43(89.6)	48(92.3)
女性	5(10.4)	4(7.7)
病程(x±s, d)	12.2±3.5	12.4±2.8	1.987^a	0.766
BMI(x±s)	22.6±2.4	22.4±1.8	0.317^a	0.752
吸烟史[例(%)]	44(91.7)	48(92.3)	0.011^b	0.906
饮酒史[例(%)]	12(25.0)	14(26.9)	0.051^b	0.826
合并症[例(%)]
高血压	34(70.8)	38(73.1)	0.060^b	0.803
糖尿病	13(27.1)	15(28.8)	0.040^b	0.845
高血脂	16(33.3)	17(32.7)	＜0.001^b	0.947
APACHE Ⅱ评分(x±s，分)	15.6±2.5	15.2±2.1	0.869^a	0.387
PaO₂(x±s, mm Hg)	53.5±8.5	52.9±9.1	0.340^a	0.735
PaCO₂(x±s，mm Hg)	74.2±11.5	74.6±10.8	0.179^a	0.858
通气方式[例(%)]			0.110^b	0.738
无创通气	8(16.7)	10(19.2)
有创通气	40(83.3)	42(80.8)
注：^a为t值，^b为χ²值。1 mm Hg=0.133 kPa。

下载: 导出CSV

表 2 2组AECOPD患者早上7点血清Mel水平比较(x±s, pg/mL)

Table 2. Comparison of serum Mel levels between two groups of patients with AECOPD at 7 a.m(x±s, pg/mL)

组别	例数	入院时	入院第5天	入院第10天	F值	P值
对照组	48	25.4±6.2	26.7±6.4	24.5±5.7	0.756	0.472
观察组	52	25.2±6.6	29.6±5.8^a	35.3±8.2^ab	3.365	0.021
t值		0.156	-2.377	-7.695
P值		0.876	0.019	＜0.001
注：与入院时比较，^aP＜0.05；与入院第5天比较，^bP＜0.05；2组组间主效应、时间主效应、组间×时间主效应的F值分别为12.536、0.342和4.623，P值分别为＜0.001、0.642和＜0.001。

下载: 导出CSV

表 3 2组AECOPD患者晚上10点血清Mel水平比较(x±s, pg/mL)

Table 3. Comparison of serum Mel levels between two groups of patients with AECOPD at 10 a.m(x±s, pg/mL)

组别	例数	入院时	入院第5天	入院第10天	F值	P值
对照组	48	45.8±9.3	46.7±9.1	44.5±7.5	0.684	0.654
观察组	52	46.1±8.5	50.8±8.5^a	55.6±6.6^ab	3.253	0.035
t值		-0.169	-2.591	-7.781
P值		0.867	0.016	＜0.001
注：与入院时比较，^aP＜0.05；与入院第5天比较，^bP＜0.05；2组组间主效应、时间主效应、组间×时间主效应的F值分别为11.635、0.354和4.536，P值分别为＜0.001、0.563和＜0.001。

下载: 导出CSV

表 4 2组AECOPD患者早上7点尿6-SMT水平比较(x±s, pg/mL)

Table 4. Comparison of urinary 6-SMT levels between two groups of patients with AECOPD at 7 a.m(x±s, pg/mL)

组别	例数	入院时	入院第5天	入院第10天	F值	P值
对照组	48	30.5±4.6	31.4±6.3	32.2±5.5	0.693	0.598
观察组	52	29.8±6.2	34.6±5.8^a	39.3±7.4^ab	3.872	0.018
t值		0.644	-2.645	-5.472
P值		0.521	0.010	＜0.001
注：与入院时比较，^aP＜0.05；与入院第5天比较，^bP＜0.05；2组组间主效应、时间主效应、组间×时间主效应的F值分别为8.634、0.253和3.728，P值分别为＜0.001、0.784和＜0.001。

下载: 导出CSV

表 5 2组AECOPD患者晚上10点尿6-SMT水平比较(x±s, pg/mL)

Table 5. Comparison of urinary 6-SMT levels between two groups of patients with AECOPD at 10 a.m(x±s, pg/mL)

组别	例数	入院时	入院第5天	入院第10天	F值	P值
对照组	48	35.7±4.7	34.4±5.2	33.6±5.2	0.563	0.737
观察组	52	36.2±6.0	38.6±5.3	42.5±7.2^ab	3.268	0.041
t值		-0.461	-3.995	-7.125
P值		0.646	＜0.001	＜0.001
注：与入院时比较，^aP＜0.05；与入院第5天比较，^bP＜0.05；2组组间主效应、时间主效应、组间×时间主效应的F值分别为10.732、0.321和4.213，P值分别为＜0.001、0.625和＜0.001。

下载: 导出CSV

表 6 2组AECOPD患者BALF中MDA水平比较(x±s, μmol/L)

Table 6. Comparison of MDA levels in BALF between two groups of patients with AECOPD(x±s, ?mol/L)

组别	例数	入院时	入院第5天	入院第10天	F值	P值
对照组	48	6.6±1.5	6.4±1.2	6.2±1.4	0.453	0.793
观察组	52	6.4±1.2	4.8±1.6^a	3.2±1.2^ab	3.165	0.046
t值		0.739	5.684	11.531
P值		0.462	＜0.001	＜0.001
注：与入院时比较，^aP＜0.05；与入院第5天比较，^bP＜0.05；2组组间主效应、时间主效应、组间×时间主效应的F值分别为12.634、0.212和4.762，P值分别为＜0.001、0.837和＜0.001。

下载: 导出CSV

表 7 2组AECOPD患者BALF中SOD水平变化比较(x±s, mU/L)

Table 7. Comparison of SOD levels in BALF between two groups of patients with AECOPD(x±s, mU/L)

组别	例数	入院时	入院第5天	入院第10天	F值	P值
对照组	48	42.5±4.2	43.5±5.2	43.6±5.3	0.572	0.718
观察组	52	42.6±3.6	49.4±6.4^a	58.3±5.0^ab	4.251	0.003
t值		-0.128	-5.034	-14.271
P值		0.898	＜0.001	＜0.001
注：与入院时比较，^aP＜0.05；与入院第5天比较，^bP＜0.05；2组组间主效应、时间主效应、组间×时间主效应的F值分别为14.262、0.353和5.736，P值分别为＜0.001、0.613和＜0.001。

下载: 导出CSV

表 8 2组AECOPD患者临床相关指标比较

Table 8. Comparison of clinical indicators of between two groups of patients with AECOPD

组别	例数	撤机成功率(%)	ICU停留时间(x±s，d)	MODS发生率(%)	28天病死率(%)
对照组	48	75.0(36/48)	14.5±3.4	37.5(18/48)	29.2(14/48)
观察组	52	94.2(49/52)	11.8±2.6	19.2(10/52)	11.5(6/52)
统计量		7.241^a	4.481^b	4.131^a	4.852^a
P值		0.007	＜0.001	0.042	0.027
注：^a为χ²值，^b为t值

下载: 导出CSV

参考文献(17)

[1]	VOGELMEIER C F, ROMAN-RODRIGUEZ M, SINGH D, et al. Goals of COPD treatment: Focus on symptoms and exacerbations[J]. Respir Med, 2020, 166(12): 105938. DOI: 10.1016/j.rmed.2020.105938.
[2]	WANG L, MENG J, WANG C, et al. Hydrogen sulfide alleviates cigarette smoke-induced COPD through inhibition of the TGF-β1/smad pathway[J]. Exp Biol Med (Maywood), 2020, 245(3): 190-200. doi: 10.1177/1535370220904342
[3]	WANG S T, BAO C, HE Y, et al. Hydrogen gas (XEN) inhalation ameliorates airway inflammation in asthma and COPD patients[J]. QJM, 2020, 113(12): 870-875. doi: 10.1093/qjmed/hcaa164
[4]	马南, 耑冰, 李萍, 等. 氧化应激失衡在支气管哮喘急性发作中的意义[J]. 中华全科医学, 2019, 17(12): 1993-1997. doi: 10.16766/j.cnki.issn.1674-4152.001110 MA N, ZHUAN B, LI P, et al. Significance of oxidative stress in acute exacerbation of bronchial asthma[J]. Chinese Journal of General Practice, 2019, 17(12): 1993-1997. doi: 10.16766/j.cnki.issn.1674-4152.001110
[5]	REITER R J, ROSALES-CORRAL S, TAN D X, et al. Melatonin as a mitochondria-targeted antioxidant: One of evolution ' s best ideas[J]. Cell Mol Life Sci, 2017, 74(21): 3863-3881. doi: 10.1007/s00018-017-2609-7
[6]	中华医学会呼吸病学分会慢性阻塞性肺疾病学组, 中国医师协会呼吸医师分会慢性阻塞性肺疾病工作委员会. 慢性阻塞性肺疾病诊治指南(2021年修订版)[J]. 中华结核和呼吸杂志, 2021, 44(3): 170-205. doi: 10.3760/cma.j.cn112147-20210109-00031 Chronic Obstructive Pulmonary Disease Group of Chinese Thoracic Society, Chronic Obstructive Pulmonary Disease Committee of Chinese Association of Chest Physician. Guidelines for the diagnosis and management of chronic obstructive pulmonary disease(revised version 2021)[J]. Chinese Journal of Tuberculosis and Respiratory Diseases, 2021, 44(3): 170-205. doi: 10.3760/cma.j.cn112147-20210109-00031
[7]	BARNES P J. Oxidative stress-based therapeutics in COPD[J]. Redox Biol, 2020, 33(6): 101544. DOI: 10.1016/j.redox.2020.101544.
[8]	吴佳萍, 陆晓玲. 尘肺并发慢性阻塞性肺疾病的危险因素分析[J]. 中华全科医学, 2020, 18(8): 1310-1312. doi: 10.16766/j.cnki.issn.1674-4152.001494 WU J P, LU X L. Risk factors analysis of pneumoconiosis complicated with chronic obstructive pulmonary disease[J]. Chinese Journal of General Practice, 2020, 18(8): 1310-1312. doi: 10.16766/j.cnki.issn.1674-4152.001494
[9]	MEHRZADI S, PORUHANIFEH M H, MIRZAEI A, et al. An updated review of mechanistic potentials of melatonin against cancer: Pivotal roles in angiogenesis, apoptosis, autophagy, endoplasmic reticulum stress and oxidative stress[J]. Cancer Cell Int, 2021, 21(1): 188. doi: 10.1186/s12935-021-01892-1
[10]	MEHRZADI M H, HOSSEINAADEH A, JUYBARI K B, et al. Melatonin and urological cancers: A new therapeutic approach[J]. Cancer Cell Int, 2020, 20(6): 444.
[11]	ZHENG Y S, TU J W, WANG X X, et al. The therapeutic effect of melatonin on GC by inducing cell apoptosis and autophagy induced by endoplasmic reticulum stress[J]. Onco Targets Ther, 2019, 12(4): 10187-10198.
[12]	MAO K M, LUO P, GENG W, et al. An integrative transcriptomic and metabolomic study revealed that melatonin plays a protective role in chronic lung inflammation by reducing necroptosis[J]. Front Immunol, 2021, 12(5): 668002. DOI: 10.3389/fimmu.2021.668002.
[13]	MORTEZAEE K. Human hepatocellular carcinoma: Protection by melatonin[J]. J Cell Physiol, 2018, 233(10): 6486-6508. doi: 10.1002/jcp.26586
[14]	BHATTACHARYA S, PATEL K K, DEHARI D, et al. Melatonin and its ubiquitous anticancer effects[J]. Mol Cell Biochem, 2019, 462(1-2): 133-155. doi: 10.1007/s11010-019-03617-5
[15]	MORTEZAEE K, KHANLARKHANI N. Melatonin application in targeting oxidative-induced liver injuries: A review[J]. J Cell Physiol, 2018, 233(5): 4015-4032. doi: 10.1002/jcp.26209
[16]	李铮, 居培红, 刘蕾蕾, 等. 褪黑素对COPD患者生物节律紊乱、T淋巴细胞亚群及肿瘤坏死因子-α的影响[J]. 海南医学, 2019, 30(20): 2594-2597. doi: 10.3969/j.issn.1003-6350.2019.20.003 LI Z, JU P H, LIU L L, et al. Effect of melatonin on biological rhythm disorder, T lymphocyte subsets, and tumor necrosis factor-α in patients with chronic obstructive pulmonary disease[J]. Hainan Medical Journal, 2019, 30(20): 2594-2597. doi: 10.3969/j.issn.1003-6350.2019.20.003
[17]	吴丹, 耿爽, 赵苏. 褪黑素对稳定期中重度慢性阻塞性肺疾病患者氧化应激和炎症反应的影响[J]. 实用医学杂志, 2017, 33(15): 2431-2435. doi: 10.3969/j.issn.1006-5725.2017.15.002 WU D, GENG S, ZHAO S. The effect of melatonin on oxidative stress and inflammatory reaction in patients with moderate to severe chronic obstructive pulmonary disease and its mechanisms[J]. The Journal of Practical Medicine, 2017, 33(15): 2431-2435. doi: 10.3969/j.issn.1006-5725.2017.15.002