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薏苡附子败酱散对TNBS结肠炎模型大鼠Treg/Th17的影响 被引量:14

Effect of Yiyi Fuzi Baijiang powder on Treg/Th17 in rats with TNBS-induced colitis
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摘要 目的:观察溃疡性结肠炎(ulcerative colitis,UC)大鼠Treg/Th17细胞的变化特点及薏苡附子败酱散对Treg/Th17的影响.方法:采用2,4,6-三硝基苯磺酸(2,4,6-trinitrob enzenesulfonic acid solution,TNBS)法制作UC大鼠模型,随机分为4组:正常组、模型组、薏苡附子败酱散(Fuzi Baijiang powder,YFB)组、阳性药美沙拉嗪缓释颗粒(positive drug mesalazine SR Granules,5-ASA)组.治疗14 d后取标本,观察肉眼形态学改变及显微镜下黏膜损伤情况,采用ELISA法测定血清中白介素-17(interleukin-17,IL-17)、IL-10活性;采用实时荧光定量PCR法检测结肠组织中RORγt、Foxp3 mRNA的表达.结果:与正常组相比,模型组大鼠结肠黏连伴肠腔扩张,肠壁增厚,组织水肿、充血,有溃疡形成.病理切片HE染色后在光镜下观察,部分黏膜出现充血坏死,肉芽组织形成,隐窝丢失,炎症细胞浸润.与模型组相比,YFB组及5-ASA组镜下病理组织评分明显降低(3.00±0.82 vs 8.00±0.82 vs 12.50±1.29,均P<0.05),血清IL-17、IL-10含量有显著差异(22.26±3.95 vs 39.62±4.26 vs 53.86±2.51,48.72±1.05 vs 44.16±1.90 vs 38.88±0.80,均P<0.05),YFB及5-ASA组间比较,YFB能显著降低IL-17含量,增加IL-10含量(均P<0.05).YFB及5-ASA组结肠组织RORγt、Foxp3 mRNA含量与模型组对比有显著差异(1.29±0.05 vs 1.32±0.87 vs 1.80±0.54;2.81±0.17 vs 2.00±0.20vs 0.47±0.04,均P<0.05),且与5-ASA组比较,YFB组RORγt mRNA含量明显下降(P<0.05),Foxp3 mRNA含量显著增加(P<0.05).结论:应用TNBS法成功建立了UC的大鼠模型.YFB能改善UC模型大鼠的炎症症状,能明显的降低结肠组织中RORγt mRNA的表达,降低血清IL-17的含量,提高Foxp3 mRNA的表达,增加IL-10的含量,YFB影响Treg/Th17细胞数量及功能是其发挥治疗溃疡性结肠炎大鼠炎症作用的机制之一. AIM: To observe the changes of Treg/Th17 in rats with ulcerative colitis (UC) and the effects of Yiyi Fuzi Baijiang powder (YFB) on Treg/Th17.METHODS: UC was induced in rats with trinitrobenzene sulfonic acid (TNBS). The rats were randomly divided into four groups: a normal group, a model group, a YFB group, and a mesalazine SR granules (5-ASA) group. Fourteen days after treatment, the rats were killed to take colonic and serum samples. Mucosal injury and microscopic morphological changes were measured. The levels of IL-17 and IL-10 in serum were determined by ELISA, and the mRNA expression of RORγt and Foxp3 was determined by RT-PCR.RESULTS: Compared with the normal group, the model group showed significant adhesion, expansion, edema, hyperemia and ulceration. Light microscopic analysis showed mucosal congestion, necrosis, granulation tissue formation, crypt loss and inflammatory cell infiltration in the model group. Compared with the model group, the microscopic pathology scores in the YFB group and 5-ASA group were significantly lower (3.00 ± 0.82, 8.00 ± 0.82 vs 12.50 ± 1.29, P 〈 0.05 for both) and serum levels of IL-17 and IL-10 were significantly altered (22.26 ± 3.95, 39.62 ± 4.26 vs 53.86 ± 2.51, 48.72 ± 1.05, 44.16 ± 1.90 vs 38.88 ± 0.80, P 〈 0.05 for all). YFB significantly reduced the levels of IL-17 and increased the levels of IL-10 compared with the 5-ASA group (P 〈 0.05 for both). The mRNA expressions of RORγt and Foxp3 in the YFB group and 5-ASA group were significantly different compared with the model group (1.29 ± 0.05, 1.32 ± 0.87 vs 1.80 ± 0.54; 2.81 ± 0.17, 2.00 ± 0.20 vs 0.47 ± 0.04, P 〈 0.05 for all). Compared with the 5-ASA group, RORγt mRNA level decreased significantly (P 〈 0.05) and Foxp3 mRNA level increased significantly (P 〈 0.05) in the YFB group.CONCLUSION: YFB can improve the symptoms of inflammation and reduce the expression of RORγt mRNA in colon tissue and the level of IL-17 in serum in rats with U
出处 《世界华人消化杂志》 CAS 北大核心 2014年第11期1542-1546,共5页 World Chinese Journal of Digestology
基金 江苏省2013年度研究生创新计划立项基金资助项目 No.CXZZ13_0612~~
关键词 薏苡附子败酱散 溃疡性结肠炎 TREG细胞 TH17细胞 Yiyi Fuzi Baijiang powder Ulcerativecolitis Treg Thl7
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参考文献15

  • 1张学洁,杨强.薏苡附子败酱散加减治疗溃疡性结肠炎[J].吉林中医药,2012,32(10):983-984. 被引量:3
  • 2曹景龙.薏苡附子败酱散加味灌肠治疗溃疡性结肠炎[J].中国民族民间医药,2010,19(21):103-103. 被引量:4
  • 3韩亮,刘昌辉.败酱草提取物对三硝基苯磺酸诱导的大鼠结肠炎的保护作用[J].广东药学院学报,2013,29(1):73-75. 被引量:17
  • 4彭金咏. 薏苡附子败酱散的药效物质基础、制备工艺及药效学研究. 第二军医大学, 2006. 被引量:1
  • 5Iba Y, Sugimoto Y, Kamei C, Masukawa T. Possiblerole of mucosal mast cells in the recovery process ofcolitis induced by dextran sulfate sodium in rats. IntImmunopharmacol 2003; 3: 485-491 [PMID: 12689654]. 被引量:1
  • 6Berrebi D, Besnard M, Fromont-Hankard G, Paris R,Mougenot JF, De Lagausie P, Emilie D, Cezard JP,Navarro J, Peuchmaur M. Interleukin-12 expressionis focally enhanced in the gastric mucosa of pediatricpatients with Crohn's disease. Am J Pathol 1998;152: 667-672 [PMID: 9502407]. 被引量:1
  • 7Parronchi P, Romagnani P, Annunziato F, SampognaroS, Becchio A, Giannarini L, Maggi E, PupilliC, Tonelli F, Romagnani S. Type 1 T-helper cell predominanceand interleukin-12 expression in the gutof patients with Crohn's disease. Am J Pathol 1997;150: 823-832 [PMID: 9060820]. 被引量:1
  • 8Heller F, Florian P, Bojarski C, Richter J, Christ M,Hillenbrand B, Mankertz J, Gitter AH, Bürgel N,Fromm M, Zeitz M, Fuss I, Strober W, Schulzke JD.Interleukin-13 is the key effector Th2 cytokine in ulcerativecolitis that affects epithelial tight junctions,apoptosis, and cell restitution. Gastroenterology 2005;129: 550-564 [PMID: 16083712]. 被引量:1
  • 9Dang EV, Barbi J, Yang HY, Jinasena D, Yu H,Zheng Y, Bordman Z, Fu J, Kim Y, Yen HR, LuoW, Zeller K, Shimoda L, Topalian SL, Semenza GL,Dang CV, Pardoll DM, Pan F. Control of T(H)17/T(reg) balance by hypoxia-inducible factor 1. Cell2011; 146: 772-784 [PMID: 21871655 DOI: 10.1016/j.cell.2011.07.033]. 被引量:1
  • 10Fujino S, Andoh A, Bamba S, Ogawa A, Hata K,Araki Y, Bamba T, Fujiyama Y. Increased expressionof interleukin 17 in inflammatory bowel disease.Gut 2003; 52: 65-70 [PMID: 12477762]. 被引量:1

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