内源性二氧化硫对脓毒症大鼠心肌氧化应激的调节

doi:10.19723/j.issn.1671-167X.2023.04.002

北京大学学报（医学版） ›› 2023, Vol. 55 ›› Issue (4): 582-586. doi: 10.19723/j.issn.1671-167X.2023.04.002

内源性二氧化硫对脓毒症大鼠心肌氧化应激的调节

刘志伟¹,刘鹏²,孟凡星³,李天水⁴,王颖¹,高嘉琪¹,周佐邑¹,王聪^1,*(),赵斌^1,*()

1. 北京积水潭医院急诊科，北京 100035
2. 北京清华长庚医院心脏内科，北京 102218
3. 北京中医医院平谷医院急诊科，北京 101200
4. 北京积水潭医院呼吸内科，北京 100035

收稿日期:2020-09-18 出版日期:2023-08-18 发布日期:2023-08-03
通讯作者: 王聪,赵斌 E-mail:congerwang1975@sina.com;zhaobin60@aliyun.com
基金资助:
北京积水潭医院青年人才培养“学科新星”计划项目(XKXX201807);北京积水潭医院自然基金培育计划项目(ZR-201927)

Regulative effects of endogenous sulfur dioxide on oxidant stress in myocardium of rat with sepsis

Zhi-wei LIU¹,Peng LIU²,Fan-xing MENG³,Tian-shui LI⁴,Ying WANG¹,Jia-qi GAO¹,Zuo-yi ZHOU¹,Cong WANG^1,*(),Bin ZHAO^1,*()

1. Department of Emergency, Beijing Jishuitan Hospital, Beijing 100035, China
2. Department of Cardiology, Beijing Tsinghua Changgung Hospital, Beijing 102218, China
3. Department of Emergency, Beijing Chinese Medicine Hospital Pinggu Hospital, Beijing 101200, China
4. Department of Respiratory Medicine, Beijing Jishuitan Hospital, Beijing 100035, China

Received:2020-09-18 Online:2023-08-18 Published:2023-08-03
Contact: Cong WANG,Bin ZHAO E-mail:congerwang1975@sina.com;zhaobin60@aliyun.com
Supported by:
the Beijing Jishuitan Hospital Nova Program(XKXX201807);the Beijing Jishuitan Hospital Natural Fund Incubation Program(ZR-201927)

摘要/Abstract

摘要：

目的: 探索内源性二氧化硫对盲肠结扎穿刺术诱导的脓毒症大鼠心肌氧化应激的调节作用。方法: 雄性Sprague Dawley大鼠40只，随机分入对照组、二氧化硫组、脓毒症组及脓毒症+二氧化硫组。检测各组大鼠血浆降钙素原(procalcitonin，PCT)、肌酸激酶同工酶(creatine kinase isoenzyme，CK-MB)、肌钙蛋白Ⅰ(cardiac Troponin Ⅰ，cTnⅠ)及脂肪酸结合蛋白(fatty acid binding protein，FABP)含量，检测各组大鼠心肌组织中过氧化氢(hydrogen peroxide，H₂O₂)含量、一氧化氮(nitric oxide，NO)含量、髓过氧化物酶(myeloperoxidase，MPO)活性、羟自由基(hydroxyl free radical，·OH)活性及丙二醛(malondialdehyde，MDA)含量，检测各组大鼠心肌组织总抗氧化能力(total antioxidant capacity，T-AOC)、过氧化氢酶(catalase，CAT)活性及细胞色素氧化酶(cytochrome oxidase，CO)含量、谷胱甘肽(glutathione，GSH)含量、谷胱甘肽氧化酶(glutathione oxidase，GSH-px)含量及超氧化物歧化酶(superoxide dismutase，SOD)活性。结果: 脓毒症时大鼠血浆PCT含量由(0.93±0.26) μg/L升高至(2.45±0.52) μg/L(P<0.01), 二氧化硫供体干预后降低至(1.58±0.36) μg/L(P<0.01)。脓毒症时大鼠血浆CK-MB、cTnⅠ及FABP含量分别由(14.46±6.48) μg/L、(151.25±30.14) ng/L及(2.72±0.65) μg/L升高至(23.72±7.72) μg/L、(272.78±52.70) ng/L及(5.22±1.01) μg/L(P均<0.01)，二氧化硫供体干预后分别降低至(16.74±3.63) μg/L、(184.86±37.72 ng/L)及(3.31±0.84) μg/L(P均<0.05)。脓毒症时大鼠心肌组织H₂O₂含量、NO含量、MPO活性、·OH活性及MDA含量分别由(67.26±8.77) mmol/g、(38.39±6.93) μmol/g、(358.25±68.12) U/g、(648.42±93.69) U/mg及(4.55±0.96) μmol/g升高至(111.45±17.35) mmol/g、(51.04±5.91) μmol/g、(465.88±76.76) U/g、(873.75±123.47) U/mg及(7.25±0.86) μmol/g(P均<0.01)。二氧化硫供体干预后分别降低至(75.99±10.52) mmol/g、(39.39±7.80) μmol/g、(393.17±51.5) U/g、(710.54±106.33) U/mg及(5.16±0.65) μmol/g(P均<0.05)。脓毒症时大鼠心肌组织T-AOC、CAT活性、CO含量、GSH含量、GSH-px含量及SOD活性分别由(2.07±0.37) U/mg、(169.25±36.86) U/g、(1.35±0.32) μmol/g、(103.51±16.62) μmol/g、(38.40±7.97) μmol/g及(38.50±8.30) U/mg降低至(1.42±0.39) U/mg、(98.44±26.56) U/g、(0.96±0.21) μmol/g、(68.05±7.35) μmol/g、(23.83±5.04) μmol/g及(23.11±4.63) U/mg(P均<0.01)。二氧化硫供体干预后分别升高至(1.83±0.37) U/mg、(146.14±31.63) U/g、(1.28±0.20) μmol/g、(92.10±11.84) μmol/g、(37.16±3.01) μmol/g及(37.29±2.62) U/mg(P均<0.05)。结论: 内源性二氧化硫在脓毒症发病过程中通过改善氧化应激平衡对心肌细胞起到保护作用。

关键词: 内源性二氧化硫, 脓毒症, 心肌损伤, 氧化应激

Abstract:

Objective: To explore the modulating effect of endogenous sulfur dioxide (SO₂) on the ba-lance of oxidation/reduction in the cecal-ligation-and-puncture-induced septic rat myocardium. Methods: Forty male Sprague Dawley rats were randomized into control group, SO₂group, sepsis group and sepsis + SO₂group. The levels of procalcitonin (PCT), creatine kinase isoenzyme (CK-MB), cardiac troponin Ⅰ (cTn Ⅰ) and fatty acid binding protein (FABP) in plasma in each group of the rats were measured; The level of hydrogen peroxide (H₂O₂), level of nitric oxide (NO), activity of myeloperoxidase (MPO), activity of hydroxyl free radical (·OH) and level of malondialdehyde (MDA) in myocardial tissue were measured; Total antioxidant capacity (T-AOC), activity of catalase (CAT), level of cytochrome oxidase (CO), level of glutathione (GSH), level of glutathione oxidase (GSH-px) and activity of superoxide dismutase (SOD) in myocardial tissue were measured. Results: The level of PCT in plasma in the rats with sepsis increased from (0.93±0.26) μg/L to (2.45±0.52) μg/L (P < 0.01), and decreased to (1.58±0.36) μg/L after the intervention of sulfur dioxide donor (P < 0.01). In sepsis, the plasma CK-MB, cTn Ⅰ and FABP levels in the rats increased respectively from (14.46±6.48) μg/L, (151.25±30.14) ng/L and (2.72±0.65) μg/L to (23.72±7.72) μg/L, (272.78±52.70) ng/L and (5.22±1.01) μg/L (P all < 0.01), and decreased to (16.74±3.63) μg/L, (184.86±37.72) μg/L and (3.31±0.84) μg/L (all P < 0.05) after the intervention of sulfur dioxide donor. The level of H₂O₂, level of NO, activity of MPO, activity of ·OH and level of MDA in myocardial tissue in the rats with sepsis increased respectively from (67.26±8.77) mmol/g, (38.39±6.93) μmol/g, (358.25±68.12) U/g, (648.42±93.69) U/ mg and (4.55±0.96) μmol/g to (111.45±17.35) mmol/g, (51.04±5.91) μmol/g, (465.88±76.76) U/g, (873.75±123.47) U/mg and (7.25±0.86) μmol/g (all P < 0.01), and decreased respectively to (75.99±10.52) mmol/g, (39.39±7.80) μmol/g, (393.17±51.5) U/g, (710.54±106.33) U/mg and (5.16±0.65) μmol/g after the intervention of the sulfur dioxide donor (all P < 0.05). The activity of T-AOC, activity of CAT, level of CO, level of GSH, level of GSH-px and activity of SOD in myocardial tissue in the rats with sepsis increased respectively from (2.07±0.37) U/mg, (169.25±36.86) U/g, (1.35±0.32) μmol/g, (103.51±16.62) μmol/g, (38.40±7.97) μmol/g and (38.50±8.30) U/mg to (1.42±0.39) U/mg, (98.44±26.56) U/g, (0.96±0.21) μmol/g, (68.05±7.35) μmol/ g, (23.83±5.04) μmol/g and (23.11±4.63) U/mg (P all < 0.01), and increased respectively to (1.83±0.37) U/mg, (146.14±31.63) U/g, (1.28±0.20) μmol/g, (92.10±11.84) μmol/g, (37.16±3.01) μmol/g and (37.29±2.62) U/mg (P all < 0.05) after the intervention of the sulfur dioxide donor. Conclusion: Endogenous SO₂ can protect rat myocardium in sepsis by modulating the ba-lance of oxidation and reduction.

Key words: Endogenous sulfur dioxide, Sepsis, Myocardic injury, Oxidant stress

中图分类号:

刘志伟,刘鹏,孟凡星,李天水,王颖,高嘉琪,周佐邑,王聪,赵斌. 内源性二氧化硫对脓毒症大鼠心肌氧化应激的调节[J]. 北京大学学报（医学版）, 2023, 55(4): 582-586.

Zhi-wei LIU,Peng LIU,Fan-xing MENG,Tian-shui LI,Ying WANG,Jia-qi GAO,Zuo-yi ZHOU,Cong WANG,Bin ZHAO. Regulative effects of endogenous sulfur dioxide on oxidant stress in myocardium of rat with sepsis[J]. Journal of Peking University (Health Sciences), 2023, 55(4): 582-586.

参考文献 18

1	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. doi: 10.1001/jama.2016.0287
2	Sun LJ , Qiao W , Xiao YJ , et al. Naringin mitigates myocardial strain and the inflammatory response in sepsis-induced myocardial dysfunction through regulation of PI3K/AKT/NF-κB pathway[J]. Int Immunopharmacol, 2019, 75, 105782. doi: 10.1016/j.intimp.2019.105782
3	Chen S , Zheng S , Liu Z , et al. Endogeous sulfur dioxide protects against oleic acid-induced acute lung injury in association with inhibition of oxidative stress in rats[J]. Lab Invest, 2015, 95 (2): 142- 156. doi: 10.1038/labinvest.2014.147
4	Siempos II , Lam HC , Ding Y , et al. Cecal ligation and puncture-induced sepsis as a model to study autophagy in mice[J]. J Vis Exp, 2014, 84, e51066.
5	Yébenes JC , Ruiz-Rodriguez JC , Ferrer R , et al. Epidemiology of sepsis in Catalonia: Analysis of incidence and outcomes in a European setting[J]. Ann Intensive Care, 2017, 7 (1): 19. doi: 10.1186/s13613-017-0241-1
6	Chambers KA , Park AY , Banuelos RC , et al. Outcomes of severe sepsis and septic shock patients after stratification by initial lactate value[J]. World J Emerg Med, 2018, 9 (2): 113- 117. doi: 10.5847/wjem.j.1920-8642.2018.02.005
7	Fu H , Wang QS , Luo Q , et al. Simvastatin inhibits apoptosis of endothelial cells induced by sepsisthrough upregulating the expression of Bcl-2 and downregulating Bax[J]. World J Emerg Med, 2014, 5 (4): 291- 297. doi: 10.5847/wjem.j.issn.1920-8642.2014.04.009
8	Gaddam RR , Fraser R , Badiei A , et al. Differential effects of kupffer cell inactivation on inflammation and the liver sieve following caecal-ligation and puncture induced sepsis in mice[J]. Shock, 2017, 47 (4): 480- 490. doi: 10.1097/SHK.0000000000000755
9	Wada K , Bunya N , Kakizaki R , et al. Successful use of veno-arterial extracorporeal membrane oxygenation for septic cardio-myopathy in a patient with pre-existing chronic heart failure[J]. Acute Med Surg, 2019, 6 (3): 301- 304.
10	孙雪莲, 肖红丽, 谭志敏, 等. 脓毒症心肌损伤患者临床特征及危险因素研究[J]. 中华急诊医学杂志, 2019, 28 (4): 494- 497.
11	张清, 李春盛. 急诊脓毒症严重程度各标记物的比较[J]. 中华急诊医学杂志, 2019, 28 (2): 163- 169.
12	Baker CC , Chaudry IH , Gaines HO , et al. Evaluation of factors affecting mortality rate after sepsis in a murine cecal ligation and puncture model[J]. Surgery, 1983, 94 (2): 331- 335.
13	Du SX , Jin HF , Bu DF , et al. Endogenously generated sulfur dioxide and its vasorelaxant effect in rats[J]. Acta Pharmacol Sin, 2008, 29 (8): 923- 930. doi: 10.1111/j.1745-7254.2008.00845.x
14	Sun Y , Tian Y , Prabha M , et al. Effects of sulfur dioxide on hypoxic pulmonary vascular structural remodeling[J]. Lab Invest, 2010, 90 (1): 68- 82. doi: 10.1038/labinvest.2009.102
15	Li Z , Huang Y , Du J , et al. Endogenous sulfur dioxide inhibits vascular calcification in association with the TGF-beta/smad signaling pathway[J]. Int J Mol Sci, 2016, 17 (3): 266. doi: 10.3390/ijms17030266
16	王海英, 吕雪雅, 刘志伟, 等. 二氧化硫对脓毒症大鼠致肺损伤炎性介质的调节[J]. 中华急诊医学杂志, 2016, 25 (6): 746- 750.
17	Zhu M , Du J , Liu AD , et al. Effect of endogenous sulfur dioxide in regulating cardiovascular oxidative stress[J]. Histol Histopathol, 2014, 29 (9): 1107- 1111.
18	Liang Y , Liu D , Ochs T , et al. Endogenous sulfur dioxide protects against isoproterenol-induced myocardial injury and increases myocardial antioxidant capacity in rats[J]. Lab Invest, 2011, 91 (1): 12- 23. doi: 10.1038/labinvest.2010.156

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内源性二氧化硫对脓毒症大鼠心肌氧化应激的调节

Regulative effects of endogenous sulfur dioxide on oxidant stress in myocardium of rat with sepsis

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