期刊文献+

布地奈德对小鼠肺组织OPN和α-SMA表达的影响及意义

Effects and Significance of Budesonide on the Expression of OPN andα-SMA in Lung Tissues of Mice
下载PDF
导出
摘要 目的观察布地奈德对呼吸道合胞病毒(respiratory syncytial virus,RSV)感染小鼠肺组织的改善效用。方法72只BALB/c小鼠随机分为对照组、观察组、干预组。对照组予生理盐水滴鼻,其余两组予106 PFU的RSV病毒液滴鼻激发,24 h后干预组予布地奈德每天1次雾化吸入30 min,其余两组予生理盐水雾化。于第4、8、14、28 d四个时间点每组随机取6只小鼠处死取标本,分析肺组织病理学改变,检测肺组织骨桥蛋白(osteopontin,OPN)和α-平滑肌肌动蛋白(α-smooth muscle actin,α-SMA)的表达。结果(1)Masson染色结果:与对照组比较,观察组及干预组在第4、8、14 d气道外周胶原沉积面积百分比明显增多(P<0.05)。与观察组比较,干预组第4、8、14 d气道外周胶原沉积面积百分比明显减少(P<0.05)。(2)OPN的表达:与对照组比较,观察组第4、8、14 d OPN表达明显增加(P<0.05),干预组第4、8 d OPN表达明显增加(P<0.05)。与观察组比较,干预组第8、14 d表达明显减少(P<0.05)。(3)α-SMA的表达:与对照组比较,干预组第4、8、14 dα-SMA表达明显增加(P<0.05)。与观察组比较,干预组第8、14 d表达明显减少(P<0.05)。结论(1)OPN与α-SMA可能参与了RSV感染小鼠气道炎症及气道胶原沉积过程;(2)布地奈德可能通过降低OPN和α-SMA的表达来减轻RSV感染引发的气道炎症及胶原沉积。 Objective To observe the improvement effect of budesonide on lung tissue of mice infected with respiratory syncytial virus(RSV).Methods 72 BALB/c mice were randomly divided into control group,observation group and intervention group.The control group was given normal saline with nasal drip,the other two groups were stimulated by nasal drops of 106 PFU RSV virus.24 h later,the intervention group was given budesonide aerosol inhalation once a day for 30min,the other two groups were atomized with normal saline.Six mice were randomly selected from each group at four time points on Day 4,Day 8,Day 14 and Day 28 and sacrificed for specimens,and analyzed the pathological changes of lung tissuea and detected the expression of OPN andα-SMA in lung tissue.Results(1)Masson staining results:Compared with the control group,the percentage of peripheral airway collagen deposition area increased in the observation group and the intervention group at the 4th,8th and 14th days(P<0.05).Compared with the observation group,the percentage of peripheral airway collagen deposition area in the 4th,8th and 14th decreased in the intervention group(P<0.05).(2)Expression of OPN:Compared with the control group,the expression of OPN was increased in the observation group on the 4th,8th and 14th days(P<0.05).The expression of OPN in the intervention group increased on day 4th and 8th(P<0.05).Compared with the observation group,the expression of the intervention group decreased on the 8th and 14th days(P<0.05).(3)The expression ofα-SMA:Compared with the control group,α-SMA expression increased in the intervention group on the 4th,8th,and 14th days(P<0.05).Compared with the observation group,the expression of the intervention group decreased on the 8th and 14th days(P<0.05).Conclusion(1)OPN andα-SMA may participate in the process of airway inflammation and collagen deposition in RSV-infected mice;(2)Budesonide may decrease the expression of OPN andα-SMA to reduce airway inflammation and collagen deposition which were caused by RSV infection.
作者 卢飞艳 宋文秀 何月贤 蒋铁汉 LU Feiyan;SONG Wenxiu;HE Yuexian;JIANG Tiehan(Department of Pediatrics,the Fifth Affiliated(Zhuhai)Hospital of Zunyi Medical University,Zhuhai Guangdong 519100,China;Department of Academic Affairs Office,the Second Clinical College of Zunyi Medical University,Zhuhai Guangdong 519100,China)
出处 《中国继续医学教育》 2022年第6期192-198,共7页 China Continuing Medical Education
基金 广东省珠海市医学科研基金资助项目(20181117 A010009)。
关键词 布地奈德 呼吸道合胞病毒 Α-平滑肌肌动蛋白 骨桥蛋白 气道重塑 气道炎症 budesonide RSV α-SMA OPN airway remodeling airway inflammation
  • 相关文献

参考文献14

二级参考文献63

  • 1Shoda H, Fujio K, Yamaguchi Yet al. Interactions between IL - 32 and tumor necrosis factor alpha contribute to the exacerbation of immune - inflammatory diseases [ J ] . Arthritis Res Ther, 2006, 8 ( 6 ) : 166.
  • 2Joosten LA, Netea MG, Kim SH et al. IL -32, a proinflammatory cytokine in rheumatoid arthritis [J].Proe Natl Acad Sci USA, 2006, 103 (9) : 3298.
  • 3Cagnard N, Letourneur F, Essabbani A et al. Interleukin - 32, CCL2, PF4F1 and GFDIO are the only cytokine/chemokine genes differentially expressed by in vitro cultured rheumatoid and osteoarthritis fibroblast - like synoviocytes [J] . Eur Cytokine Netw, 2005, 16 (4) : 289.
  • 4Shioya M, Nishida A, Yagi Yet al. Epithelial overexpression of interleukin - 32 - alpha in inflammatory bowel disease [ J] . Clin Exp Immunol, 2007, 149 (3): 480.
  • 5Kim KH, Shim JH, Seo EH et al. Interleukin - 32 monoclonal antibodies for immunohistochemistry, Western blotting, and ELISA [J]. J Immunol Methods, 2008, 333 (1-2): 38.
  • 6Du Q, Chen Z, Zhou LF et al. Inhibitory effects of astragaloside IV on ovalbumin-induced chronic experimental asthma [J] . Can J Physiol Pharmacol, 2008, 86 (7) : 449.
  • 7Rydell Trmanen K, Uller L, Erjefalt JS. Remodeling of extra - bronchial lung vasculature following allergic airway inflammation [ J ] . Respir Res, 2008, 9:18.
  • 8Coda C, Kanaji T, Kanaji Set al. Involvement of IL -32 in activation induceded cell death in T ceils[J] . International Immunology, 2006, 18 (2): 233.
  • 9Obase Y, Shimoda T, Milsula K et al. Correlaction between airway hyperresponsiveness and airway inflammation in a young adult population: eosinophil, ECP, and cytokine levels in induced sputum [J].. Ann Allergy Asthma Immunol, 2001, 86 (3) : 304.
  • 10Susumu Nakae, Carolina Lunderius. TNF can contribute to muhiple features of ovalbumin - induced allergic inflammation of the airways in mice [J]. J Allergy Clin Immunol, 2007, 119 (3) : 680.

共引文献276

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部