中药对溃疡性结肠炎相关炎性因子和信号通路的影响探析
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摘要
溃疡性结肠炎是一种以溃疡为主要症状的慢性非特异性肠道疾病,属于中医"痢疾""肠风""便血"等范畴。西医治疗以氨基水杨酸、糖皮质激素等为主,存在疗效不理想、复发率较高、副作用较大的问题。近年来中药治疗溃疡性结肠炎取得了较好的临床效果,有副作用小、不良反应少、复发率低的优点,可以明显改善UC患者症状,提高其生活质量。中医中药对肠黏膜的免疫调控影响也获得了较多关注,中药对与UC相关信号传导通路的干预作用逐渐成为研究热点。本文将常见与UC相关的信号传导通路进行归纳,探究青黛、大黄、姜黄对其影响,为临床和实验研究提供思路。
Colitis gravis is a chronic nonspecific intestinal disease with the prime symptom of intestinal ulcer,which is belonged to the category of dysentery,intestinal wind and blood stool in traditional Chinese medicine.While the prime treatment of western medicine is aminosalicylic acid,glucocorticoid,etc,there also existing the problems of unsatisfactory curative effect,high recurrence rate and great side effects.In recent years,Chinese medicine for colitis gravis has achieved a pretty wonderful clinical effect,with the advantage of small side effects,less adverse reactions and low recurrence rate,which could significantly improve the condition of UC patients and enhance the quality of life.The influence of traditional Chinese medicine on the immunoregulation of intestinal mucosa has also received more attention,and the intervention of traditional Chinese medicine towards UC-related inflammatory factors and signal transduction pathways has been gradually becoming a hot topic.
Colitis gravis is a chronic nonspecific intestinal disease with the prime symptom of intestinal ulcer,which is belonged to the category of dysentery,intestinal wind and blood stool in traditional Chinese medicine.While the prime treatment of western medicine is aminosalicylic acid,glucocorticoid,etc,there also existing the problems of unsatisfactory curative effect,high recurrence rate and great side effects.In recent years,Chinese medicine for colitis gravis has achieved a pretty wonderful clinical effect,with the advantage of small side effects,less adverse reactions and low recurrence rate,which could significantly improve the condition of UC patients and enhance the quality of life.The influence of traditional Chinese medicine on the immunoregulation of intestinal mucosa has also received more attention,and the intervention of traditional Chinese medicine towards UC-related inflammatory factors and signal transduction pathways has been gradually becoming a hot topic.
引文
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[2]Oyama Y,Craig RM,Traynor AE,et al.Autologous hematopoietic stem cell transplantation in patients with refractory Crohn's disease[J].Gastroenterology,2005,128(3):552-563.
[3]Cassinotti A,Annaloro C,Ardizzone S,et al.Autologous haematopoietic stem cell transplantation without CD34+cell selection in refractory Crohn’s disease[J].Gut,2008,57(2):211-217.
[4]陈津,马予洁,黄梁浒,等.年龄对人骨髓间充质干细胞分离培养的影响[J].实用医学杂志,2010,26(20):3694-3697.
[5]Richter J M,Schanbacher B L,Huang H,et al.Lipopolysaccharide binding protein enables intestinal epithelial restitution despite lipopolysaccharide exposure[J].J Pediatric Gastroenterol Nutr,2012,54(5):639-644.
[6]Coskun M,Salem M,Pedersen J,et al.Involvement of JAK/STAT signaling in the pathogenesis of inflammatory bowel disease[J].Pharmacol Res,2013,76:1-8.
[7]时美静,李睿岩,张玉彬,中药治疗溃疡性结肠炎所涉信号通路研究进展[J].药学进展,2016,40(8):610-618.
[8]赵青春,沈洪,程海波,等.清肠化湿方对HT-29细胞IL-6/JAK2/STAT3的影响[J].中国药理学通报,2015,31(6):883-885.
[9]Eastaff-Leung N,Mabarrack N,Barbour A,et al.Foxp3+regulatory T cells,Th17 effector cells,and cytokine environment in inflammatory bowel disease[J].J Clin Immunol,2010,30(1):80-89
[10]闫曙光,惠毅,李京涛,等.Notch信号通路与溃疡性结肠炎的相关研究进展[J].重庆医学,2015,44(35):5033-5035.
[11]姜鹏君,孙雪梅,陈敏,等.青黛提取物对HEL细胞增殖、凋亡和分化的影响[J].中国生化药物杂志,2011,32(3):190-193.
[12]刘丽娟,王志斌,王允亮,等.青黛对实验性结肠炎抗炎作用的体内外研究[J].北京中医药大学学报,2014,37(10):691-695+3.
[13]胡鸿毅,马贵同,朱凌云,等.三七、青黛等对溃疡性结肠炎组织中核因子NF-κB活性的影响[J].上海中医药大学学报,2007(5):44-48.
[14]周联.大黄素等中药单体对HT-29细胞TLR4表达及MAPKs信号通路的影响[D].广州:广州中医药大学,2006.
[15]郭振军.大黄多糖治疗溃疡性结肠炎的机制研究[D].西安:第四军医大学,2013.
[16]Rezaie A,Parker R D,Abdollahi M.Oxidative Stress and Pathogenesis of Inflammatory Bowel Disease:An Epiphenomenon or the Cause?[J].Digestive Diseases&Sciences,2007,52(9):2015.
[17]廖辉.姜黄素对溃疡性结肠炎大鼠的抗炎作用及其对肠黏膜IL-23的影响[D].西宁:广西医科大学,2012.
[18]Zhaojing Z,Lingling Z,Hui L,et al.Curcumin improves TNBS-induced colitis in rats by inhibiting IL-27 expression via the TLR4/NF-κB signaling pathway.[J].Planta Medica,2013,79(2):102.