肠吉泰对肠易激综合征内脏高敏感大鼠结肠黏膜炎性细胞因子的影响
|
摘要
目的观察肠吉泰对肠易激综合征(IBS)内脏高敏感大鼠结肠黏膜炎性细胞因子的影响。方法将50只新生期SD大鼠随机分为5组:正常组、模型组、得舒特组、肠吉泰低剂量组、高剂量组各10只,用醋酸刺激法建立IBS内脏高敏感大鼠模型,并予以相应药物治疗。治疗4周后,采用直肠球囊扩张法测定其内脏敏感性,ELISA法测定结肠黏膜白介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)和白介素-10(IL-10)的表达。结果与正常组相比,模型组内脏敏感性升高(P<0.01);模型组结肠黏膜IL-1β、TNF-α表达明显升高(P<0.01),IL-10表达明显降低(P<0.05);与模型组比较,肠吉泰各组和得舒特组内脏高敏感性明显降低(P<0.01),肠吉泰高剂量组大鼠结肠粘膜促炎细胞因子IL-1β、TNF-α的表达性明显降低(P<0.05, P<0.01),结肠黏膜抗炎细胞因子细胞IL-10升高(P<0.01);得舒特组结肠黏膜IL-1β、TNF-α和IL-10的表达与模型组无显著差别(P>0.05)。结论高剂量的肠吉泰可以降低IBS大鼠的内脏高敏感性,其机制可能与调整结肠黏膜炎性细胞因子的平衡有关。
Objective To observe the effect of Changjitai on colonic mucosal inflammatory cytokines in irritable bowel syndrome(IBS) rats with visceral hypersensitivity. Methods Fifty neonatal Sprague-Dawley rats were randomly divided into normal control group, model control group, Dicetel group, Changjitai low-dose group and high-dose group, 10 in each group.The IBS rats model with visceral hypersensitivity was induced by intrarectal acetic acid irritation in the latter 4 groups. The corresponding drugs were administrated. After 4-week treatment, rectal balloon distension was applied to evaluate visceral hypersensitivity. The levels of IL-1β, TNF-α and IL-10 in colonic mucosa were detected by ELISA. Results Compared with normal control group, the visceral sensitivity of model control group was significantly increased(P<0.01). The expression of IL-1β and TNF-a in model control group was significantly higher in colonic mucosa than that in normal control group(P<0.01), and the expression of IL-10 in model control group was significantly lower in colonic mucosa than that in normal control group(P<0.05).Compared with model control group,the visceral sensitivity of Changjitai group and Dicetel group were significantly lower(P<0.01). The expression of IL-1β and TNF-α in Changjitai high-dose group was significantly lower in colonic mucosa than that in model control group(P<0.05, P<0.01), and the expression of IL-10 in Changjitai high-dose group was significantly higher in colonic mucosa than that in model control group(P<0.01).There were no significant difference between Dicetel group and model control group in the levels of IL-1β, TNF-α and IL-10(P>0.05). Conclusion High-dose Changjitai can reduce the visceral hypersensitivity by regulating the balance of colonic mucosal inflammatory cytokines.
Objective To observe the effect of Changjitai on colonic mucosal inflammatory cytokines in irritable bowel syndrome(IBS) rats with visceral hypersensitivity. Methods Fifty neonatal Sprague-Dawley rats were randomly divided into normal control group, model control group, Dicetel group, Changjitai low-dose group and high-dose group, 10 in each group.The IBS rats model with visceral hypersensitivity was induced by intrarectal acetic acid irritation in the latter 4 groups. The corresponding drugs were administrated. After 4-week treatment, rectal balloon distension was applied to evaluate visceral hypersensitivity. The levels of IL-1β, TNF-α and IL-10 in colonic mucosa were detected by ELISA. Results Compared with normal control group, the visceral sensitivity of model control group was significantly increased(P<0.01). The expression of IL-1β and TNF-a in model control group was significantly higher in colonic mucosa than that in normal control group(P<0.01), and the expression of IL-10 in model control group was significantly lower in colonic mucosa than that in normal control group(P<0.05).Compared with model control group,the visceral sensitivity of Changjitai group and Dicetel group were significantly lower(P<0.01). The expression of IL-1β and TNF-α in Changjitai high-dose group was significantly lower in colonic mucosa than that in model control group(P<0.05, P<0.01), and the expression of IL-10 in Changjitai high-dose group was significantly higher in colonic mucosa than that in model control group(P<0.01).There were no significant difference between Dicetel group and model control group in the levels of IL-1β, TNF-α and IL-10(P>0.05). Conclusion High-dose Changjitai can reduce the visceral hypersensitivity by regulating the balance of colonic mucosal inflammatory cytokines.
引文
[1]Canavan C,West J,Card T.The epidemiology of irritable bowel syndrome[J].Clin Epidemiol,2014(6):71-80.
[2]熊理守,陈旻湖,陈惠新,等.广东省社区人群肠易激综合征的流行病学研究[J].中华医学杂志,2004,84(4):278-281.
[3]Ford AC,Talley NJ.Mucosal inflammation as a potential etiological factor in irritable bowel syndrome:a systematic review[J].Gastroenterol,2011,46(4):421-431.
[4]陈奇.中药药理研究方法学[M].2版.北京:人民卫生出版社,2006:31.
[5]张正利,王莹,李典典.肠吉泰治疗腹泻型肠易激综合征临床观察[J].上海中医药大学学报,2012,26(5):41-44.
[6]Ortiz-Lucas M,Saz-Peiro P,Sebastian-Domingo JJ.Irritable bowel syndrome immune hypothesis.Part two:the role of cytokines[J].Rev Esp Enferm Dig,2010,102(12):711-717.
[7]Gwee KA,Collins SM,Read NW,et al.Increased rectal mucosal expression of interleukin 1beta in recently acquired post-infectious irritable bowel syndrome[J].Gut,2003,52(4):523-526.
[8]Chang L,Adeyemo M,Karagiannides I,et al.Serum and colonic mucosal immune markers in irritable bowel syndrome[J].Am J Gastroenterol,2012,107(2):262-272.
[9]Bashashati M,Rezaei N,Bashashati H,et al.Cytokine gene polymorphisms are associated with irritable bowel syndrome:a systematic review and meta-analysis[J].Neurogastroenterol Motil,2012,24(12):1102-e566.
[10]黄小平,刘欣,王燕,等.肠易激综合征患者炎性细胞因子与claudin-1的相关性[J].山西医科大学学报,2015,46(9):876-880.
[11]Bashashati M,Rezaei N,Shafieyoun A,et al.Cytokine imbalance in irritable bowel syndrome:a systematic review and meta-analysis[J].Neurogastroenterol Motil,2014,26(7):1036-1048.
[12]李延青,于岩波.神经-免疫调节在肠易激综合征腹痛发生机制中的研究进展[J].国际消化病杂志,2012,32(2):65-67.
[2]熊理守,陈旻湖,陈惠新,等.广东省社区人群肠易激综合征的流行病学研究[J].中华医学杂志,2004,84(4):278-281.
[3]Ford AC,Talley NJ.Mucosal inflammation as a potential etiological factor in irritable bowel syndrome:a systematic review[J].Gastroenterol,2011,46(4):421-431.
[4]陈奇.中药药理研究方法学[M].2版.北京:人民卫生出版社,2006:31.
[5]张正利,王莹,李典典.肠吉泰治疗腹泻型肠易激综合征临床观察[J].上海中医药大学学报,2012,26(5):41-44.
[6]Ortiz-Lucas M,Saz-Peiro P,Sebastian-Domingo JJ.Irritable bowel syndrome immune hypothesis.Part two:the role of cytokines[J].Rev Esp Enferm Dig,2010,102(12):711-717.
[7]Gwee KA,Collins SM,Read NW,et al.Increased rectal mucosal expression of interleukin 1beta in recently acquired post-infectious irritable bowel syndrome[J].Gut,2003,52(4):523-526.
[8]Chang L,Adeyemo M,Karagiannides I,et al.Serum and colonic mucosal immune markers in irritable bowel syndrome[J].Am J Gastroenterol,2012,107(2):262-272.
[9]Bashashati M,Rezaei N,Bashashati H,et al.Cytokine gene polymorphisms are associated with irritable bowel syndrome:a systematic review and meta-analysis[J].Neurogastroenterol Motil,2012,24(12):1102-e566.
[10]黄小平,刘欣,王燕,等.肠易激综合征患者炎性细胞因子与claudin-1的相关性[J].山西医科大学学报,2015,46(9):876-880.
[11]Bashashati M,Rezaei N,Shafieyoun A,et al.Cytokine imbalance in irritable bowel syndrome:a systematic review and meta-analysis[J].Neurogastroenterol Motil,2014,26(7):1036-1048.
[12]李延青,于岩波.神经-免疫调节在肠易激综合征腹痛发生机制中的研究进展[J].国际消化病杂志,2012,32(2):65-67.