芍药汤对溃疡性结肠炎大鼠肠黏膜免疫屏障的干预作用
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摘要
目的:探讨芍药汤对2,4,6-三硝基苯磺酸(TNBS)诱导的溃疡性结肠炎大鼠肠黏膜免疫屏障的影响。方法:将60只SD大鼠随机分为正常组,模型组,美沙拉嗪组(0.067 g·kg~(-1)),芍药汤低、中、高剂量组(1.8,3.6,7.2 g·kg~(-1)),采用TNBS诱导溃疡性结肠炎模型,对应给予生理盐水、美沙拉嗪、芍药汤灌胃治疗7 d,采用苏木素-伊红(HE)染色观察结肠组织病理学改变,免疫组化法和蛋白免疫印迹法(Western blot)检测肠黏膜中CD4~+T淋巴细胞数量和分泌型免疫球蛋白A(SIg A)蛋白的表达。结果:与正常组比较,模型组大鼠肠黏膜损伤程度评分及病理学评分显著升高(P<0.01);CD4~+T淋巴细胞,SIg A蛋白表达显著下降(P<0.01);与模型组比较,各给药组大鼠结肠黏膜损伤程度评分及病理学评分显著下降(P<0.01),肠黏膜CD4~+T淋巴细胞,SIg A表达明显升高(P<0.05,P<0.01);与美沙拉嗪组及芍药汤低剂量组比较,芍药汤中、高剂量组肠黏膜损伤程度评分和病理学评分显著下降(P<0.01),芍药汤中、高剂量组大鼠肠黏膜中CD4~+T淋巴细胞及SIg A蛋白表达明显升高(P<0.05)。结论:芍药汤可通过增加肠黏膜中CD4~+T细胞数量及SIg A分泌的表达,起到减轻肠黏膜损伤,保护肠黏膜免疫屏障功能作用。
Objective: To investigate effect of Shaoyaotang on intestinal mucosal immune barrier induced by 2,4,6-trinitrobenzene sulphonic acid( TNBS) in rats with ulcerative colitis. Method: Sixty SD rats were randomly divided into normal group,model group,mesalazine group( 0. 067 mg·kg~(-1)),low,medium and highdose Shaoyaotang groups( 1. 8,3. 6,7. 2 g·kg~(-1)). In the TNBS-induced ulcerative colitis model,saline,mesalazine,peony soup were administered by gavage for 7 days. Hematoxylin-eosin( HE) staining was used to detect the histopathological changes of colon tissue. The number of CD4~+T lymphocytes and the expression of secretory immunoglobulin A( SIg A) in intestinal mucosa were detected by immunohistochemistry and Western blot. Result: Compared with normal group,the scores of intestinal mucosal injury and the pathological scores in model group increased significantly( P < 0. 01). The expressions of CD4~+T lymphocytes and SIg A in the intestinal mucosa of model group decreased significantly( P < 0. 01). Compared with model group,the scores of colonic mucosal damage and the pathological scores decreased significantly in rats( P < 0. 01). The expressions of CD4~+T lymphocytes and SIg A in the intestinal mucosa of rats in each group elevated significantly( P < 0. 05,P < 0. 01).Compared with mesalazine group and low-dose Shaoyaotang group,the intestinal mucosal injury score and the pathological scores in medium and high-dose Shaoyaotang groups decreased significantly( P < 0. 01). The expression levels of CD4~+T lymphocytes and SIg A protein in the intestinal mucosa of rats in middle and high doses Shaoyaotang groups increased significantly( P < 0. 05). Conclusion: Shaoyaotang can reduce the intestinal mucosal damage and protect the intestinal mucosal immune barrier by increasing the number of CD4~+T cells and the expression of SIg A secretion in the intestinal mucosa.
Objective: To investigate effect of Shaoyaotang on intestinal mucosal immune barrier induced by 2,4,6-trinitrobenzene sulphonic acid( TNBS) in rats with ulcerative colitis. Method: Sixty SD rats were randomly divided into normal group,model group,mesalazine group( 0. 067 mg·kg~(-1)),low,medium and highdose Shaoyaotang groups( 1. 8,3. 6,7. 2 g·kg~(-1)). In the TNBS-induced ulcerative colitis model,saline,mesalazine,peony soup were administered by gavage for 7 days. Hematoxylin-eosin( HE) staining was used to detect the histopathological changes of colon tissue. The number of CD4~+T lymphocytes and the expression of secretory immunoglobulin A( SIg A) in intestinal mucosa were detected by immunohistochemistry and Western blot. Result: Compared with normal group,the scores of intestinal mucosal injury and the pathological scores in model group increased significantly( P < 0. 01). The expressions of CD4~+T lymphocytes and SIg A in the intestinal mucosa of model group decreased significantly( P < 0. 01). Compared with model group,the scores of colonic mucosal damage and the pathological scores decreased significantly in rats( P < 0. 01). The expressions of CD4~+T lymphocytes and SIg A in the intestinal mucosa of rats in each group elevated significantly( P < 0. 05,P < 0. 01).Compared with mesalazine group and low-dose Shaoyaotang group,the intestinal mucosal injury score and the pathological scores in medium and high-dose Shaoyaotang groups decreased significantly( P < 0. 01). The expression levels of CD4~+T lymphocytes and SIg A protein in the intestinal mucosa of rats in middle and high doses Shaoyaotang groups increased significantly( P < 0. 05). Conclusion: Shaoyaotang can reduce the intestinal mucosal damage and protect the intestinal mucosal immune barrier by increasing the number of CD4~+T cells and the expression of SIg A secretion in the intestinal mucosa.
引文
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[20]SANG L X,CHANG B,ZHU J F,et al.Sodium selenite ameliorates dextran sulfate sodium-induced chronic colitis in mice by decreasing Th1,Th17,andγδT and increasing CD4(+)CD25(+)regulatory T-cell responses[J].World J Gastroenterol,2017,23(21):3850-3863.
[21]CUI Y,ZHU C,MING Z,et al.Molecular mechanisms by which casein glycomacropeptide maintains internal homeostasis in mice with experimental ulcerative colitis[J].PLo S One,2017,doi:10.1371/journal.pone.0181075.
[22]王移飞,赵党生,王凤仪,等.芍药汤调节湿热型溃疡性结肠炎大鼠JAK2/STAT3和SOC3的分子机制[J].中国实验方剂学杂志,2017,23(23):97-102.
[2]戴路明,朱磊,沈洪.基于β2AR/β-arrestin2/NF-κB信号通路的清肠化湿颗粒防治溃疡性结肠炎的作用机制[J].中国实验方剂学杂志,2018,24(9):86-94.
[3]周文鹏,白爱平.炎症性肠病常见基因多态性[J].胃肠病学,2018,23(3):177-180.
[4]WANG K,WU L Y,DOU C Z,et al.Research advance in intestinal mucosal barrier and pathogenesis of crohn's disease[J].Gastroenterol Res Pract,2016,doi:10.1155/2016/9686238.
[5]MA T M,XU N,MA X D,et al.Moxibustion regulates inflammatory mediators and colonic mucosal barrier in ulcerative colitis rats[J].World J Gastroenterol,2016,22(8):2566-2575.
[6]Vancamelbeke M,Vermeire S.The intestinal barrier:a fundamental role in health and disease[J].Expert Rev Gastroenterol Hepatol,2017,11(9):821-834.
[7]YU X T,XU Y F,HUANG Y F,et al.Berberrubine attenuates mucosal lesions and inflammation in dextran sodium sulfate-induced colitis in mice[J].PLo S One,2018,doi:10.1371/journal.pone.0194069.
[8]罗丹,仝战旗.中医药治疗溃疡性结肠炎的临床研究进展[J].医学综述,2017,23(2):336-339,343.
[9]齐雪阳,张勤生,张春燕.芍药汤加减保留灌肠联合美沙拉嗪肠溶片治疗大肠湿热证溃疡性结肠炎[J].中国实验方剂学杂志,2016,22(19):149-153.
[10]夏修文,陈桥桥,丁斗,等.芍药汤治疗溃疡性结肠炎的作用机制研究进展[J].成都中医药大学学报,2018,41(3):119-123.
[11]李冀,连建伟.方剂学[M].北京:中国中医药出版社,2016:89-90.
[12]LU Y,LIN H,ZHANG J,et al.Sijunzi Decoction attenuates 2,4,6-trinitrobenzene sulfonic acid(TNBS)-induced colitis in rats and ameliorates TNBSinduced claudin-2 damage via NF-κB pathway in Caco2cells[J].BMC Complement Altern Med,2017,17(1):35.
[13]赵欣,恽海峰,向桂玲,等.白头翁汤加减联合双歧杆菌制剂对大鼠溃疡性结肠炎的影响[J].中国实验方剂学杂志,2018,24(13):110-116.
[14]贺石林,王键,王净净.中国科研设计与统计学[M].长沙:湖南科学技术出版社,2013:48.
[15]XU B,LIU X L,DONG W W,et al.EGCG maintains Th1/Th2 balance and mitigates ulcerative colitis induced by dextran sulfate sodium through TLR4/My D88/NF-κB signaling pathway in rats[J].Can J Gastroenterol Hepatol,2017,doi:10.1155/2017/3057268.
[16]HOU Y,LU X,ZHANG Y.IRAK inhibitor protects the intestinal tract of necrotizing enterocolitis by inhibiting the Toll-like receptor(TLR)inflammatory signaling pathway in rats[J].Med Sci Monit,2018,24:3366-3373.
[17]孙健,高文艳,林一帆.溃疡性结肠炎病因和发病机制研究进展[J].辽宁中医药大学学报,2017,19(4):94-97.
[18]Rogler G,Andus T.Cytokines in inflammatory bowel disease[J].World J Surg,1998,22(4):382-389.
[19]YU W,LU B,ZHANG H,et al.Effects of the Sijunzi decoction on the immunological function in rats with dextran sulfate-induced ulcerative colitis[J].Biomed Rep,2016,5(1):83-86.
[20]SANG L X,CHANG B,ZHU J F,et al.Sodium selenite ameliorates dextran sulfate sodium-induced chronic colitis in mice by decreasing Th1,Th17,andγδT and increasing CD4(+)CD25(+)regulatory T-cell responses[J].World J Gastroenterol,2017,23(21):3850-3863.
[21]CUI Y,ZHU C,MING Z,et al.Molecular mechanisms by which casein glycomacropeptide maintains internal homeostasis in mice with experimental ulcerative colitis[J].PLo S One,2017,doi:10.1371/journal.pone.0181075.
[22]王移飞,赵党生,王凤仪,等.芍药汤调节湿热型溃疡性结肠炎大鼠JAK2/STAT3和SOC3的分子机制[J].中国实验方剂学杂志,2017,23(23):97-102.
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