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Relationship between differential gene expression in pure oxygen and air pulmonary ventilation relating to lung injury |
CHEN Chao1 LI Yuntao2 ZHANG Hongbo3 SHEN Liang4 NIE Xiaohu2 WEI Pengxiang5 |
1.Department of Anesthesia, Huzhou Central Hospital Affiliated Central Hospital of Huzhou University, Zhejiang Province, Huzhou 313000, China;
2.Department of Neurosurgery, Huzhou Central Hospital Affiliated Central Hospital of Huzhou University, Zhejiang Province, Huzhou 313000, China;
3.Department of Neurosurgery, Zhujiang Hospital, Southern Medical University, Guangdong Province, Guangzhou 510000, China;
4.Department of Neurosurgery, the Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Jiangsu Province, Changzhou 213000, China; 5.Department of Neurosurgery, Beihai People’s Hospital, Guangxi Zhuang Autonomous Region, Beihai 536000, China |
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Abstract Objective To explore the relationship between differential gene expression in pure oxygen and air pulmonary ventilation relating to lung injury. Methods Five Rattus norvegicus rats were randomly assigned to the experiment group (pure oxygen ventilations, n = 3) and the control group (air ventilation, n = 2). The R software was used to analyze the differential gene expression of lung tissues between the two groups, and functional enrichment was used to analyze differential gene function, protein-protein interactions were constructed to visualize and visualize the protein network of differential genes. Results There were 140 differential genes expressed in the lung tissues of two groups. The differential gene function was mainly enriched in mitochondria, mitochondrial respiratory chain complex Ⅰ, activation of homologous dimer proteins, intercellular connection and exosomes, among which mitochondria respiratory chain complex Ⅰ was a low-expression gene, which include NDUFB3, NDUFA4, NDUFB1, NDUFB9, NDUFB10, NDUFC1 and NDUFC2, respectively. Conclusion Lung injury under high oxygen content ventilation mainly inhibits the synthesis of ATP in mitochondrial respiratory chain complex Ⅰ. NDUFA4, NDUFB1, NDUFB3, NDUFB9, NDUFB10, NDUFC1, and NDUFC2 genes are the major differential genes in oxidative stress injury and play an important role in lung injury.
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[1] Boehm O,Rohner M,Ehrentraut H,et al. Low-tidal-volume prevent ventilation induced inflammation in a mouse model of sepsis [J]. Life Sci,2020,240:117081.
[2] Sahetya SK. Searching for the optimal positive end-expiratory pressure for lung protective ventilation [J]. Curr Opin Crit Care,2020,26(1):53-56.
[3] van der Woude MC,Bormans L,van der Horst RP,et al. Pulmonary levels of biomarkers for inflammation and lung injury in protective versus conventional one-lung ventilation for oesophagectomy:A randomised clinical trial [J]. Eur J Anaesthesiol,2020,37(11):1040-1049.
[4] 张才军,谢俊然,肖旺频,等.个体化保护性肺通气策略对老年患者全身麻醉肺通气效果的影响[J].中华实验外科杂志,2019,36(8):1475-1478.
[5] Li H,Wang G,Lin S,et al. Loss of interleukin-6 enhances the inflammatory response associated with hyperoxia-induced lung injury in neonatal mice [J]. Exp Ther Med,2019,17(4):3101-3107.
[6] Fu C,Dai X,Yang Y,et al. Dexmedetomidine attenuates lipopolysaccharide-induced acute lung injury by inhibiting oxidative stress,mitochondrial dysfunction and apoptosis in rats [J]. Mol Med Rep,2017,15(1):131-138.
[7] Ma J,Wang Y,Wu Q,et al. Seawater immersion aggravates burn-associated lung injury and inflammatory and oxidative-stress responses [J]. Burns,2017,43(5):1011-1020.
[8] Shen H,Wu N,Wang Y,et al. Chloroquine attenuates paraquat-induced lung injury in mice by altering inflammation,oxidative stress and fibrosis [J]. Int Immunopharmacol,2017,46:16-22.
[9] Vasanthi RS,Kinal NV,Jessica AC,et al. Protective Role of Surfactant Protein-D Against Lung Injury and Oxidative Stress Induced by Nitrogen Mustard [J]. Toxicol Sci,2018, 166(1):108-122.
[10] Koksal GM,Dikmen Y,Erbabacan E,et al. Hyperoxic oxidative stress during abdominal surgery:A randomized trial [J]. J Anesth,2016,30(4):610-619.
[11] Wang SH,Li LH,Zou DM,et al. Roles of the mammalian target of rapamycin(mtor)signaling pathway in the repair of hyperoxia-induced acute lung injury [J]. Adv Clin Exp Med,2020,21(1):13-23.
[12] Fisher AO,Husain K,Wolfson MR,et al. Hyperoxia during one lung ventilation:Inflammatory and oxidative responses [J]. Pediatr Pulmonol,2012,47(10):979-986.
[13] 李凤杰,沈丽君,方合志,等.线粒体呼吸链复合体Ⅰ[J].中国细胞生物学学报,2014,36(8):1153-1161.
[14] 徐婷,李华,鲁姗姗,等.线粒体电子传递呼吸链及其生物学意义的研究进展[J].复旦学报:医学版,2015,42(2):250-255,261.
[15] Yu S,Shi M,Liu C,et al. Time course changes of oxidative stress and inflammation in hyperoxia-induced acute lung injury in rats [J]. Iran J Basic Med Sci,2015,18(1):98-103.
[16] 蔡成,常立文.线粒体呼吸链与新生儿高氧肺损伤[J].国际儿科学杂志,2008(3):202-204.
[17] Sch?覿gger H,Pfeiffer K. Supercomplexes in the respiratory chains of yeast and mammalian mitochondria [J]. EMBO J,2000,19(8):1777-1783.
[18] Wu W,Yan L,Chen S,et al. Investigating oxidation state-induced toxicity of pegylated graphene oxide in ocular tissue using gene expression profiles [J]. Nanotoxicology,2018,12(8):819-835.
[19] Rubattu S,Stanzione R,Volpe M. Mitochondrial dysfunction contributes to hypertensive target organ damage:Lessons from an animal model of human disease [J]. Oxid Med Cell Longev,2016,2016:1067801.
[20] Yagil C,Varadi-Levi R,Yagil Y. A novel mutation in the nadh dehydrogenase(ubiquinone)1 alpha subcomplex 4(ndufa4)gene links mitochondrial dysfunction to the development of diabetes in a rodent model [J]. Dis Model Mech,2018,11(11):dmm036699.
[21] 李廷坤,李长生,吕帅国,等.小潮气量快频率双肺通气辅以二氧化碳气胸用于胸腔镜食管癌根治术患者气道管理的效果[J].中华麻醉学杂志,2017,37(1):96-99.
[22] 李彭依,王丽君,许仄平,等.单肺通气时吸入不同浓度氧对食管癌根治术患者氧合及氧化应激反应的影响[J].中华临床医师杂志:电子版,2017,11(6):909-913.
[23] 张亚楠,黎笔熙,殷桂林,等.内皮素-1受体拮抗剂对兔单侧肺通气时肺损伤的保护作用[J].中华实验外科杂志,2019,36(7):1232-1235.
[24] 张亚楠.内皮素-1受体拮抗剂bq-123预处理对兔单侧肺通气时肺损伤的保护及pi3k-akt-hif-1α信号通路的影响[D].广州:南方医科大学,2018.
[25] 倪小磊,黄祥.七氟烷联合丙泊酚麻醉对单肺通气的肺保护作用及血清icam-1、hmgb1水平的影响[J].国际呼吸杂志,2019,39(10):776-781. |
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