期刊文献+
任意字段
题名或关键词
题名
关键词
文摘
作者
第一作者
机构
刊名
分类号
参考文献
作者简介
基金资助
栏目信息

甘草酸对白细胞介素13诱导的大鼠气道黏液高分泌的作用 被引量：5

Effects of glycyrrhizin on airway mucus hypersecretion induced by interleukin-13 in rats
原文传递
导出
摘要 目的探讨甘草酸对白细胞介素13（IL-13）诱导的气道黏液高分泌的作用。方法sD大鼠50只用随机数字表法随机分为5组：对照组、IL-13组和不同浓度（25、50、75mg／kg）甘草酸组。通过黏液组化染色，采用形态定量法计算气道上皮组织染色阳性部分表达强度积分；体外培养人支气管上皮细胞株HBE-16细胞，分为6组：阴性对照组（生理盐水）、IL-13对照组（10斗∥L的IL-13±生理盐水）和不同浓度甘草酸干预组（10μg/L的IL-13分别加25、50、75μmol／L甘草酸）、阳性对照组（10μg／L的IL-13±25μmol／L唑泊司他），通过反转录-PCR、Western印迹、荧光法和活性氧细胞渗透性指示剂（CM—H。DCFDA）探针的荧光强度分别检测各组HBE-16细胞黏蛋白（MUC）5ACmRNA、MUC5AC蛋白表达及细胞内的醛糖还原酶（AR）活性和活性氧（ROS）相对表达水平。结果体内实验：各组气道上皮组织染色阳性细胞表达强度积分分别为0．12±0．03、0．87±0．13、0．56±0．08、0．46±0．06、0．35±0．04，不同浓度甘草酸组明显低于IL-13组（均P〈0．05），并有剂量依赖性；IL-13组明显强于对照组（P〈0．05）。体外实验：各组HBEl6细胞的AR活性及48h时的ROS相对表达水平分别为0．156±0．021、0．692±0．039、0．436±0．019、0．323±0．042、0．290±0．027和5．127±0．033、24．257±3．263、11．966±0．283、8．892±0．521、6．426±0．173，IL-13对照组明显高于阴性对照组（P〈0．05），不同浓度甘草酸干预组明显低于IL．13对照组（均P〈0．05）；各组HBEl6细胞MUC5ACmRNA和MUC5AC蛋白表达分别为0．82±0．05、3．22±0．12、2．57±0．34、2．09±0．54、1．58±0．22和0．18±0．04、0．65±0．15、0．48±0．11、0．33±0．19、0．26±0．06，IL-13对照组明显高于阴性对照组（P〈0．05），不同浓度甘草酸干预组明显低于IL-13对照组（均P〈0．05）。结论甘草酸可抑制IL-13诱导的MUC5ACmRNA和蛋白质的表达，抑制气道黏液高分泌。 Objective To explore the effects of glycyrrhizin on airway mucus hypersecretion induced by interleukin-13 （ IL-13 ） in rats. Methods A total of 50 SD rats were divided randomly into 5 groups with a random digit table： control group, IL-13 group, and different dosage （25, 50, 75 mg/kg） glycyrrhizin groups. The integral of expression intensity in positive cells of airway epithelium under mucus histochemical stain was calculated with modality-quantitative method. HBE-16 cells were divided into 6 groups： negative control （physiological saline）, IL-13 control （10 μg/L IL-13 ± physiological saline）, different concentration glycyrrhizin interference （10 μg/L IL-13 ± 25, 50 and 75 μmol/L glycyrrhizin, respectively） and positive control （ 10 μg/L IL-13 ± 25 p.moi/L zopolrestat）. The expression of mucin （MUC） 5AC mRNA, MUC5AC protein, aldose reductase （AR） activity and reactive oxygen species （ROS） content were detected by reverse transcription-polymerase chain reaction （RT-PCR） , Western blot, fluorometric method and fluorescence intensity with General Oxidative Stress Indicator （CM-H2DFDA） catheter respectively. Results In vivo, the integral of expression intensity in positive stain cells of airwayepithelium were 0. 12 ±0. 03,0. 87±0. 13, 0. 56 ±0. 08, 0. 46 ±0. 06 and 0. 35 ±0. 04 respectively while the integral of different dosage glycyrrhizin groups was significantly lower than that of [L-13 group （ all P 〈 0. 05） with dose depentency and the IL-13 group was stronger than control group （P 〈0. 05）. In vitro, the index of AR activity and ROS at 48 h of HBE16 cells in every group were 0. 156 ±0. 021, 0. 692 ±0. 039, 0. 436 ±0. 019, 0. 323 ± 0. 042 and 0. 290 ± 0. 027; 5. 127 ± 0. 033, 24. 257± 3. 263, 11. 966 ± 0. 283, 8. 892 ±0. 521 and 6. 426 ±0. 173 respectively. The indices of IL-13 control group were higher than those of negative control group （ P 〈 0. 05 ） while those of different concentration glycyrrhizin interference groups were lower than those of IL-13 control group （all P 〈0. 05）. The expressions of MUC5AC mRNA and protein of HBE16 cells in every group were 0. 82±0. 05, 3.22 ±0. 12, 2. 57 ±0. 34, 2. 09±0. 54 and I. 58±0. 22; 0. 18 ±0. 04, 0. 65 ±0. 15, 0.48 ±0. 11 , 0. 33 ±0. 19 and O. 26 ±0. 06 respectively. The indices of IL-13 control group were higher than those of negative control group （P 〈 0. 05 ） and those of different concentration glyeyrrhizin interferenee groups were lower than those of IL-13 control group （ P 〈0. 05 ）. Conclusion Glycyrrhizin may inhibit the expression of MUC5AC mRNA and MUC5AC protein induced by IL-13 and control the hvpersecretion of airway mucus.
作者 童瑾 周向东 尤列·皮尔曼 维克多·科罗索夫
机构地区 重庆医科大学附属第二医院呼吸内科 俄罗斯医学科学院远东呼吸生理与病理研究中心
出处 《中华医学杂志》 CAS CSCD 北大核心 2013年第28期2225-2229,共5页 National Medical Journal of China
基金 国家自然科学基金（31171346）
关键词 甘草酸 醛还原酶 白细胞介素13 黏蛋白类 Glycyrrhizie acid Aldehyde reductase Interleukin-13 Mucins
分类号 R285.5 [医药卫生—中药学]
  • 相关文献

参考文献13

  • 1Barqaqli E,Olivieri C,Bennett D, et al. Oxidative stress in thepathogenesis of diffuse lung diseases : a review. Respir Med,2009, 103: 1245-1256.
  • 2周佳,尤列·皮尔曼,维克多·科罗索夫,周向东.神经调节蛋白1β在白细胞介素1β所致气道黏液高分泌中的作用[J].中华医学杂志,2012,92(28):1988-1991. 被引量：8
  • 3Muthenna P,Suryanarayana P,Gunda SK,et al. Inhibition ofaldose reductase by dietary antioxidant curcumin : mechanism ofinhibition, specificity and significance. FEBS Lett, 2009 , 583 :3637-3642.
  • 4Tsuge M, Goto S, Kato F, et al. Elevation of serum transaminaseswith norovirus infection. Clin Pediatr ( Phila),2010,49: 574-578.
  • 5李敏超,尤列·皮尔曼,维克多·科罗索夫,周向东.冷空气联合香烟烟雾吸入诱导大鼠气道黏液高分泌的机制及药物的干预作用[J].中华医学杂志,2012,92(32):2283-2287. 被引量：5
  • 6Yadav UC, Aguilera-Aguirre L, Ramana KV, et al. Aldosereductase inhibition prevents metaplasia of airway epithelial cells.PLoS One, 2010, 5: el4440.
  • 7Yadav UC, Naura AS, Aguilera-Aguirre L, et al. Aldosereductase inhibition suppresses the expression of Th2 cytokines andairway inflammation in ovalbumin- induced asthma in mice. JImmonol, 2009 , 183 : 4723-4732.
  • 8强丽霞,金寿德,唐昊,李兵,修清玉,石昭泉.TIM-1对哮喘小鼠气道MUC5AC及Th2细胞因子表达的影响[J].第二军医大学学报,2012,33(6):581-584. 被引量：3
  • 9Yu H, Li Q, Kolosov VP, et al. Interleukin-13 induces mucin5AC production involving STAT6/SPDEF in human airwayepithelial cells. Cell Commu Adhes, 2010,17 : 83-92.
  • 10Sikora JP, Chlebna-Sok6t D, Andrzejewska E, et al. Clinicalevaluation of proinflammatory cytokine inhibitors ( STNFR I,STNFR II,IL-la) , anti-inflammatory cytokines (IL-10, IL-13 )and activation of neutrophils after bum-induce inflammation.Scand J Immonol, 2008,68 : 145-152.

二级参考文献32

  • 1张永,程德云,王慧,苏巧俐,陈小菊,关键.慢性阻塞性肺疾病大鼠肺内白细胞介素-8和肿瘤坏死因子-α与气道炎症的关系研究[J].中国呼吸与危重监护杂志,2003,2(6):355-359. 被引量：41
  • 2Kuyper L M,Parfi P D, Hogg J C, Lambert R K, Ionescu D, Woods R, et al. Characterization of airway plugging in fatal asthma[J]. Am J Med, 2003,115 . 6-11.
  • 3Rose M C,Voynow J A. Respiratory tract mucin genes and mu- cin glycoproteins in health and disease[J]. Physiol Rev, 2006, 86:245-278.
  • 4Evans C M,Kim K,Tuvim M J,17)ickey B F. Mucus hypersecre tion in asthma: causes and effects [J]. Curr opin Pulm Med, 2009,15:4-11.
  • 5Freeman G J,Casasnovas J M,Umetsu D T,DeKruyff R H. TIM genes: a family of cell surface phosphatidylserine recep tots that regulate innate and adaptive immunity[J]. Immune Rev,2010,235 : 172-189.
  • 6Whittaker L,Niu N,Temann U A,Stoddard A,Flavell R A, Ray A, et al. Interleukin-13 mediates a fundamental pathway for airway epithelial mucus induced by CD4 T cells and inter leukin-9[J]. Am J Respir Cell Mol Biol, 2002,27 : 593-602.
  • 7Lee M Y,Seo C S,Lee N H,Ha H,Lee J A,Lee H,et al. Anti asthmatic effect of sehizandrin on OVA induced airway inflam mation in a murine asthma model [J].Int hnmunopharmacol, 2010,10:1374-1379.
  • 8Kirkham S, Sheehan J K, Knight D, Richardson P S, Thornton D J. Heterogeneity of airways mucus: variations in the a mounts and glyco{orms of the major oligomeric mucins MUCSAC and MUC5B [J]. Biochem J, 2002,361 (Pt 3) : 537-546.
  • 9Tan Y F,Zhang W,Yang L,Jiang S P. The effect of formotero on airway goblet cell hyperplasia and protein Mue5ac expres sion in asthmatic mice[J]. Eur Rev Med Pharmacol Soil,2011 15, 743-750.
  • 10Young H W, Williams O W, Chandra D Bellinghausen 1. K, P6rez G,Suarez A,et al. Central role of Muc5ac expression in mucous metaplasia and its regulation by conserved 5 , elements [J]. Am J Respir Cell Mol Biol,2007,37:273-290.

共引文献12

同被引文献30

  • 1慢性阻塞性肺疾病诊治指南(2013年修订版)[J].中国医学前沿杂志（电子版）,2014,6(2):67-80. 被引量：2038
  • 2Rogers DF. Physiology of airway mucus secretion and pathophysiology of hypersecretion[J]. Respir Care, 2007, 52 (9) : 1134-1146; discussion 1146-1149.
  • 3Martin C, Frija-MassonJ, Burgel PRo Targeting mucus hypersecretion: new therapeutic opportunities for COPD?[J] . Drugs, 2014, 74 (10): 1073-1089. DOl: 10.1007/s40265- 014-0235-3.
  • 4Inagaki-Ohara K, Kondo T, Ito M, et al. SOCS, inflammation, and cancer[J].JAKSTAT, 2013, 2 (3): e24053. DOl: 10. 41611jkst.24053.
  • 5Ahmed CM, LarkinJ 3rd,Johnson HM. SOCSI Mimetics and Antagonists: A Complementary Approach to Positive and Negative Regulation of Immune Function[J]. Front Immunol, 20 15, 6: 183. DOl: 10. 3389/fimmu. 2015. 00183.
  • 6Li W, Yan F, Zhou H, et al. P. aeruginosa lipopolysaccharide?induced MUC5AC and CLCA3 expression is partly through Duoxl in vitro and in vivo[IJ. PLoS One, 2013, 8 (5): e63945. DOl: 10. 13711joumal. pone. 0063945.
  • 7Endo TA, Masuhara M, Y okouchi M, et al. A new protein containing an SH2 domain that inhibitsJAK kinases[J]. Nature, 1997,387(6636): 921-924. DOl: 10.1038/43213.
  • 8Yoshimura A, Naka T, Kubo M. SOCS proteins, cytokine signalling and immune regulation[J]. Nat Rev Immunol, 2007 , 7(6): 454465. DOl: 10.1038/nri2093.
  • 9Gielen V, Sykes A, ZhuJ, et al. Increased nuclear suppressor of cytokine signaling I in asthmatic bronchial epithelium suppresses rhinovirus induction of innate interferons[J].J Allergy Clin Immunol, 2015, 136 (I): 177-188. DOl: 10. 1016/j.Jaci. 2014.11. 039.
  • 10LennerzJK, Hoffmann K, Bubolz AM, et al. Suppressor of cytokine signaling I gene mutation status as a prognostic biomarker in classical Hodgkin lymphoma[J]. Oncotarget, 2015,6(30): 29097 -2911 O. DOl: 10. 18632/oncotarget. 4829.

引证文献5

二级引证文献40

中华医学杂志
2013年 第28期

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