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SAM对大鼠自身免疫性肺气肿氧化应激的干预

Intervention of S-adenosyl-L-methionine on oxidative stress in rats with autoimmune emphysema
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摘要 目的:探讨S-腺苷甲硫氨酸(S-adenosyl-l-methionine,SAM)对大鼠自身免疫性肺气肿氧化应激的干预作用。方法:将30只10周龄雄性清洁级SD大鼠随机分为3组:健康对照组(n=10)、肺气肿组(n=10)、SAM组(n=10)。参照文献将原代培养人脐静脉内皮细胞及完全弗氏佐剂注入肺气肿组及SAM组大鼠腹腔,健康对照组只给予完全弗氏佐剂注射。SAM组大鼠还腹腔注射SAM 15 mg/(kg·d)。21 d后,3组大鼠均取右肺组织切片行HE染色观察病理学改变,并定量测定肺平均内衬间隔(mean linear intercept,MLI)、平均肺泡数(mean alveolar number,MAN)。以分光光度剂分别检测血清中的丙二醛(malondialdehyde content,MDA)浓度,超氧化物歧化酶(superoxide dismutase,SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)活力及谷胱甘肽(glutathione,GSH)浓度。以ELISA法检测血清中抗内皮细胞抗体(anti-endothelial cell antibody,AECA)浓度。结果:肺气肿组MLI较健康对照组增加,其MAN较佐剂组减少,而SAM组MLI、MAN均介于2组之间,差异具有统计学意义(均P=0.000)。肺气肿组GSH浓度、GSH-Px活力、SOD活力较健康对照组均降低(均P=0.000),SAM组上述指标均介于2组之间(P=0.000)。肺气肿组MDA浓度较健康对照组升高(P=0.000),SAM组MDA浓度介于2组之间(P=0.000)。结论:SAM可能通过提高血清中GSH含量及GSH-Px、SOD活力,降低MDA浓度水平抑制大鼠自身免疫性肺气肿的形成。 Objective:To study the intervention effect of S-adenosyl-L-methionine(SAM)on oxidative stress in rats with autoimmune emphysema.Methods:Thirty SD male rats with age of ten weeks were randomly divided into three groups:the normal control group(n=10),the emphysema group(n=10)and the SAM group(n=10).Rats in the emphysema group and the SAM group were treated with intraperitoneal injection of human umbilical vein endothelial cells plus complete Freund’s adjuvant to establish autoimmune emphysema models,while in the normal control group were treated with intraperitoneal injection of the same dosage complete Freund’s adjuvant.In addition,rats in the SAM group were also treated with intraperitoneal injection of SAM of 15 mg/(kg·d).After 21 days,tissue sections of right lung were stained by hematoxylin eosin(HE),pathological changes were observed,and mean linear intercept(MLI)and mean alveolar number(MAN)were measured.At the same time,malondialdehyde(MDA),superoxide dismutase(SOD),activities of glutathione peroxidase(GSH-Px),and the glutathione(GSH)in serum were detected by the spectrophotometry.Levels of antiendothelial cell antibody(AECA)in serum were detected by using ELISA.Results:MLI in the emphysema group was higher than that in the normal control group,MAN in the emphysema group was lower than that in the normal control group,while MLI and MAN in the SAM group were both in the middle when compared with those two groups,with statistically significant differences(P=0.000;P=0.000).GSH concentration,SOD activity,and GSH-Px activity in the emphysema group were decreased than those in the normal control group(P=0.000;P=0.000;P=0.000),while in the the SAM group were in the middle when comparedwith those two groups(P=0.000).MDA concentration in the emphysema group was higher than that in the normal control group,while in the SAM group were in the middle when compared with those two groups(P=0.000).Conclusion:SAM may inhibit the formation of autoimmune emphysema in rats by increasing the production of GSH concentration,SOD activity,and GSH-Px activity,and decreasing the level of MDA.
作者 张野 张程 李夏 李本雪 李佳艺 张湘燕 林洁如 Zhang Ye;Zhang Cheng;Li Xia;Li Benxue;Li Jiayi;Zhang Xiangyan;Lin Jieru(Department of Respiratory and Critical Medicine,Guizhou Provincial People’s Hospital,NHC Key Laboratory of Pulmonary Immunological Diseases)
出处 《重庆医科大学学报》 CAS CSCD 北大核心 2020年第11期1528-1531,共4页 Journal of Chongqing Medical University
基金 国家自然科学基金资助项目(编号:81560012) 贵州省科技计划资助项目(编号:黔科合〔2016〕支撑2907、黔科合基础〔2017〕1100) 筑科合同(〔20151001〕社78号、〔20161001〕09号)。
关键词 氧化应激 自身免疫性肺气肿 S-腺苷甲硫氨酸 抗内皮细胞抗体 大鼠 oxidative stress autoimmune emphysema S-adenosyl-L-methionine anti-endothelial cell antibody rat
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  • 1黄俊芳,王广发.慢性阻塞性肺病全球倡议慢性阻塞性肺病指南(2013更新版)解读[J].中国医学前沿杂志(电子版),2013,5(3):58-60. 被引量:60
  • 2金哲,王广发.慢性阻塞性肺疾病全球倡议(2014更新版)解读[J].中国医学前沿杂志(电子版),2014,6(2):94-97. 被引量:140
  • 3吴纪珍,马利军,李素云,牛红丽.慢性阻塞性肺疾病发作期与缓解期体内胶原、细胞因子变化及临床意义[J].中国实用内科杂志,2005,25(8):703-704. 被引量:37
  • 4Hanania NA,Marciniuk DD. A unified front against COPD:clinical practice guidelines from the American College of Physicians, the American College of Chest Physicians, the American Thoracic Society, and the European Respiratory Society. Chest, 2011,140 : 565 -566.
  • 5Pourfarzam S, Ghazanfari T, Yaraee R, et al. Serum levels of IL-8 and IL-6 in the long term pulmonary complications induced by sulfur mustard : Sardasht-Iran Cohort Study. Int Immunophar:lacol, 2009, 9 : 1482-1488.
  • 6Wood LG, Gibson PG, Garg ML. Biomarkers of lipid peroxidation, airway inflammation and asthma. Eur Respir J,2003,211 :177-186.
  • 7Churg A, Dai J, Tai H, et al. Tumor necrosis factor-alpha is central to acute cigarette smoke-induced inflammation and connective tissue breakdown. Am J Respir Crit Care Med ,2002,166:849-854.
  • 8Mayer R J, Marshall LA. New insights on mammalian phospholipase A2 ( s ), comparison of arachidonoyl-selective and -nonselective enzymes. FASEB J, 1993,7:339-348.
  • 9Kim DK, Fukuda T, Thompson BT, et al. Bronchoalveolar lavage fluid phospholipase A2 activities are increased in human adult respiratory distress syndrome. Am J Physiol, 1995,269 ( 1 Pt 1 ) : L109-L118.
  • 10Currie GP, Rossiter C, Miles SA, et al. Effects of tiotropium and other long acting bronchodilators in chronic obstructive pulmonary disease. Pulm Pharmacol Ther,2006,19 : 112-119.

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