加味白头翁汤对溃疡性结肠炎大鼠结肠粘膜损伤修复作用的机理研究
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摘要
目的
溃疡性结肠炎(UC)的病因和发病机制目前还不十分清楚。近年来,随着对溃疡性结肠炎研究的深入,人们对溃疡性结肠炎发病及治疗有了新的认识,认为不论是肠道的原发性病变,还是继发性损害,均会造成结肠粘膜结构和功能的损伤,肠粘膜损伤与溃疡性结肠炎发病密切相关。肠粘膜不仅是营养物质消化、吸收的重要场所,同时也是致病微生物和毒素侵入的主要门户。生理情况下,机体可通过肠粘膜屏障来有效地阻止致病微生物和毒素的侵入,以保证机体处于健康状态。当肠粘膜屏障损伤时,肠道中的微生物和毒素便可突破肠粘膜屏障,进入门静脉和淋巴系统引起细菌移位,甚至发展为溃疡性结肠炎。
为明确炎性细胞调控因子NF-κB、β-防御素-2、TFF3、EGF及TGF-β1在肠道自我保护和损伤后修复机制中的重要地位,本课题采用高脂高糖饮食加上TNBS灌肠法复制湿热型溃疡性结肠炎大鼠模型,在结肠粘膜损伤方面“寻本溯源”,把研究的重点放在炎性细胞调控因子NF-κB及p-防御素-2上。在肠道修复作用方面,则重点探讨TFF3、EGF、TGF-β1在溃疡性结肠炎发生发展及粘膜修复过程中的变化及相关调节机制。通过观察加味白头翁汤对NF-κB活化及β-防御素-2、TFF3、TGFβ1、EGF表达的影响,进而探讨加味白头翁汤对溃疡性结肠炎肠道损伤修复的作用机理。从而为加味白头翁汤应用于溃疡性结肠炎临床提供理论基础,同时对中医治则治法的现代化研究作有益探讨。
方法
将40只SPF级健康SD大鼠,雌雄各半,随机分为正常对照组、模型组、柳氮磺胺吡啶组、加味白头翁汤组,每组10只。采用三硝基苯磺酸([NBS)局部灌肠加高脂高糖法建立UC大鼠模型,动物模型制作成功后,中药治疗组给予加味白头翁汤灌胃,西药对照组给予柳氮磺胺吡啶(SASP)灌胃,模型组及正常对照组给予等容积的生理盐水灌胃,每天1次,连用15d。治疗结束后将大鼠固定于鼠解剖台上,腹腔注射20%氨基甲酸乙酯麻醉,剖取整个结肠组织,先行肉眼仔细观察各组大鼠结肠粘膜的充血、水肿、伪膜、溃疡和糜烂数目及面积病理改变情况,然后再取少量结肠粘膜组织石蜡包埋,HE染色,光镜观察大鼠结肠组织病理形态学变化。剩余结肠粘膜标本运用蛋白免疫印迹(Western blot)法检测NF-κB的蛋白表达水平,用Real-time PCR方法测定β-防御素-2、TFF3的基因表达变化,免疫组化法观察TGFβ1、EGF蛋白表达的变化。
结果
1加味白头翁汤方组与模型组相比较：大鼠的一般情况明显好转,大鼠脓血便和粘液便消失,大便成形,活动灵活,食欲好转,大鼠体重明显增高。加味白头翁汤方可使结肠粘膜组织损伤和病理组织学评分降低,与模型组比较,差异显著(P<0．01)。结肠粘膜组织的充血、水肿、伪膜、溃疡和糜烂数目及面积减少,肠壁损伤修复,炎性细胞浸润减少,溃疡附近肠粘膜可见不连续粘液层覆盖,而粘膜下层则可见胶原纤维增生。
2与正常组比较,模型组大鼠NF-KB p65表达显著增高,差异显著(P<0.01)；给予加味白头翁汤治疗后,NF-KB p65表达明显下降,与模型组比较,差异显著(P<0.01)；中药治疗组与西药对照组比较无显著差异(P>0.05)。
3与正常组比较,模型组大鼠结肠粘膜β-防御素-2表达显著增高,差异显著(P<0.01)；给予加味白头翁汤治疗后,结肠粘膜β-防御素-2基因表达明显下降,与模型组比较,差异显著(P<0.01),中药治疗组与西药对照组比较无显著差异(P>0.05)。
4与正常组比较,模型组大鼠结肠粘膜TFF3略有降低,但没有显著差异(P>0.05)；给予加味白头翁汤治疗后,结肠粘膜TFF3基因表达明显上升,与模型组比较,差异显著(P<0.01)；中药治疗组与西药对照组比较无显著差异(P>0.05)。
5与正常组比较,模型组TGF β1的表达明显增高,两组比较差异显著(P<0.01),给予加味白头翁汤治疗后,TGF β1相对表达明显下降,与模型组比较,差异显著(P<0.01),中药治疗组与西药对照组比较无显著差异(P>0.05)。与正常组比较,模型组EGF的表达明显低于正常组,两组比较差异显著(P<0.01)；给予加味白头翁汤治疗后,EGF蛋白相对表达明显增高,与模型组比较,差异显著(P<0.01),中药治疗组与西药对照组比较无显著差异(P>0.05)。
结论
1加味白头翁汤方可抑制UC的炎性细胞浸润,使炎症减轻,同时还有促进结肠粘膜损伤修复,恢复结肠粘膜的分泌功能的作用。说明本课题UC模型复制成功。加味白头翁汤方可通过减轻结肠炎症,促进结肠粘膜修复,从而起到治疗UC的作用。
2NF-KB p65的表达与UC病情严重性和活动性之间有一定关系,提示UC结肠粘膜组织的NF-KB表达水平可反映结肠组织的损害程度,对于病情评估和治疗效果判断可能具有潜在指导意义。加味白头翁汤组对UC大鼠模型过度激活的NF-KB有抑制作用,这可能是加味白头翁汤组治疗UC大鼠的作用机理之一。
3加味白头翁汤方的治疗作用可能在于通过下调β-防御素-2基因表达含量,进而减轻结肠粘膜的炎症反应,杀伤肠道病原微生物,起到粘膜修复的作用。β-防御素-2可能是加味白头翁汤治疗UC作用的关键的靶位。
4加味白头翁汤方可通过增加结肠上皮细胞TFF3的分泌从而促进受损结肠粘膜组织的修复。
5加味白头翁汤对UC大鼠模型结肠粘膜TGF β1蛋白表达有下调作用,从而抑制炎症的发生发展；对UC大鼠EGF的蛋白表达则有上调作用,能够促进受损粘膜周围的完好上皮细胞向损伤粘膜表面迁移覆盖,加快损伤粘膜的修复。
Objective
The etiology and pathogenesis of ulcerative colitis (UC) is not very clear. In recent years, with in-depth study of ulcerative colitis, the incidence and treatment of ulcerative colitis have a new understanding that regardless of the primary lesion of the intestinal tract, or consequential damages, would result in the colon closely related to the mucous membrane structure and function of injury in the pathogenesis of ulcerative colitis. Mucosa is not only an important place of nutrient digestion and absorption but also pathogenic microorganisms and toxins to invade the main portal.Under physiological conditions, the body through the mucosal barrier to effectively prevent the invasion of pathogenic microorganisms and toxins in order to ensure that the body in a healthy state. Microorganisms and toxins can break through the intestinal mucosal barrier into the portal vein and the lymphatic system. They also can cause bacterial translocationand the development of ulcerative colitis.
To explicit inflammatory cells regulating factor of NF-κB, β-defensin-2, TFF3,EGF and TGF-beta in intestinal self-protection and damage repair mechanisms, the subject of high-fat high-sugar diet plus TNBS enema copy ulcerative colitis rat model and tracking them back in the colonic mucosa damage, the study focused on the regulation ofinflammatory cell factor NF-κB transcription factor. In the intestinal repairing, the study focused on the β-defensin-2, TFF3and EGF and TGF-beta in the Ulcerative Colitis change and relatedregulation mechanism in the development and mucosal repair process. Through observation the Modified Pulsatilla Decoction on the NF-κB activation and β-defensin-2, TFF3and TGFβ1,EGF expression, and then explore the intestinal injury and repair mechanism of the Added Pulsatilla Decoction on ulcerative colitis, and to provide theoretical foundation on Added Pulsatilla Decoction used in ulcerative colitis clinical.
Methods
40of SPF health SD rats were randomly divided into normal control group, model group,the sulfasalazine group, Added Pulsatilla Decoction group.(N=10). Trinitrobenzene sulfonic acid (TNBS) local enema plus high fat and sugar established the UC rat model. After the success of produced Animal model,the treatment group given modified the Pulsatilla soup gavage, the comparison group given sulfasalazine (SASP) orally once a day, model group and normal control group given the same volume of of normal saline once a15d. After end of treatment, rats were fixed on the rat of dissecting table, the intraperitoneal injection of20%urethane anesthesia, dissected the entire colon tissue, first carefully observed by the naked eye the colonic mucosa of rats in each group congestion, edema, pseudomembranous, ulcers and erosions.The number and size of the pathological changes, and then take a small amount of colonic mucosa tissue embedded in paraffin, HE staining and observed by light microscopy, the pathological changes of rat colon tissue. The remaining colonic mucosa specimens using Western blot (Western blot analysis) assay of NF-κB protein expression levels, Real-time PCR method for determination of (3-defensins-2TFF3gene expression changes in the immunohistochemical method observation of TGFβ1and EGF changes in protein expression.
Results
1Compared with model group, the general situation in Added Pulsatilla Decoction group was significantly improved, in rat blood and pus and mucus disappeared, stool forming, flexible activities, improved appetite, body weight of rats was significantly higher. Added Pulsatilla Decoction group can make the intestine mucosal injury and histological score lower, compared with model group, the difference was significant (P<0.01). Intestine mucosal congestion, edema, pseudomembranous, ulcers, and erosion number and size were reduced, intestinal damage were repaired, inflammatory cell infiltration were reduced, ulcer mucosa can be seen near continuous mucus layer covering the submucosa visible collagen fibers.
2Compared with normal group, the model group rats of NF-KB of p65expression significantly with increased,(P<0.01); given to the treatment of Added Pulsatilla Decoction, NF-κB of p65expression was significantly decreased, compared with model group, the differences was significant (P <0.01); treatment group and comparison group showed no significant differences (P>0.05).
3Compared with normal group, model group rats colonic mucosa beta-defensin-2expression was significantly higher, the difference was significant (P<0.01); give Added Pulsatilla Decoction treatment, the colonic mucosa beta-defensin-2gene expression was significantly decreased. Compared with model group, the difference was significant (P<0.01), treatment group and comparison group showed no significant difference (P>0.05).
4Compared with the normal group, the model group rat colonic mucosa ITF decreased slightly, but no significant differences (P>0.05); given Added Pulsatilla Decoction treatment, the colonic mucosa TFF3gene expression increased significantly compared with the model group, the difference was significant (P<0.01); treatment group and comparison group showed no significant difference (P>0.05).
5Compared with the normal group, model group TGFβ1of expression was significantly increased, the differences was significant (P<0.01), to give Added Pulsatilla Decoction treatment of TGFβ1is relatively express the amount for the significantly decreased, compared with model group,the differences was significant (P<0.01), treatment group and western medicine in the control group showed no significant difference (P>0.05). Compared with the normal group, model group, EGF expression was significantly lower than the normal group, the difference was significant (P<0.01); give Added Pulsatilla Decoction treatment of EGF protein relative expression was significantly increased compared with model group, the difference was significant (P<0.01), treatment group and comparison group showed no significant difference (P>0.05).
Conclusion
1The Added Pulsatilla Decoction can inhibit the inflammatory cell infiltration of the UC, reduced the inflammation, as well as promote the repair of the colonic mucosa damage and restore the secretory function of the colonic mucosa. The model of UC were copied successfully. The Added Pulsatilla Decoction can reduce colonic inflammation, promote colonic mucosa repair, and thus play a role in the treatment of UC.
2Have a certain relationship between the NF-κB p65expression and UC disease severity and activity, suggesting that the organization of the UC colonic mucosa of NF-KBexpression level may reflect the extent of damage of the colon tissue, the judgment of the condition assessment and treatment effects may potentially guidance. The Added Pulsatilla Decoction can inhibit the excessive activation of NF-KB on UC rat model, which may be one of the mechanisms of the Added Pulsatilla Decoction group on the treatment of UC rats.
3The Added Pulsatilla Decoction of therapeutic effect may be that the content by down-regulating β-defensin-2gene expression, and thus reduce the inflammation of thecolonic mucosa, destruction of intestinal pathogenic microorganisms, play a role inmucosal repair. beta-defensin-2may be the role of key target by Added Pulsatilla Decoction treatment of UC
4The Added Pulsatilla Decoction can increase the TFF3secretion in the colonic epithelial cells and to promote tissue repair of the damaged colonic mucosa.
5The Added Pulsatilla Decoction can downward TGF(31protein expression of the UC rat,and inhibit the inflammation development. The Added Pulsatilla Decoction can increase the EGF protein expression of UC rat, can contribute to the damaged mucous membrane surrounding the integrity of the epithelial cells to injury the migration of the mucosal surface coverage, accelerate the repair of damaged mucosa.
溃疡性结肠炎(UC)的病因和发病机制目前还不十分清楚。近年来,随着对溃疡性结肠炎研究的深入,人们对溃疡性结肠炎发病及治疗有了新的认识,认为不论是肠道的原发性病变,还是继发性损害,均会造成结肠粘膜结构和功能的损伤,肠粘膜损伤与溃疡性结肠炎发病密切相关。肠粘膜不仅是营养物质消化、吸收的重要场所,同时也是致病微生物和毒素侵入的主要门户。生理情况下,机体可通过肠粘膜屏障来有效地阻止致病微生物和毒素的侵入,以保证机体处于健康状态。当肠粘膜屏障损伤时,肠道中的微生物和毒素便可突破肠粘膜屏障,进入门静脉和淋巴系统引起细菌移位,甚至发展为溃疡性结肠炎。
为明确炎性细胞调控因子NF-κB、β-防御素-2、TFF3、EGF及TGF-β1在肠道自我保护和损伤后修复机制中的重要地位,本课题采用高脂高糖饮食加上TNBS灌肠法复制湿热型溃疡性结肠炎大鼠模型,在结肠粘膜损伤方面“寻本溯源”,把研究的重点放在炎性细胞调控因子NF-κB及p-防御素-2上。在肠道修复作用方面,则重点探讨TFF3、EGF、TGF-β1在溃疡性结肠炎发生发展及粘膜修复过程中的变化及相关调节机制。通过观察加味白头翁汤对NF-κB活化及β-防御素-2、TFF3、TGFβ1、EGF表达的影响,进而探讨加味白头翁汤对溃疡性结肠炎肠道损伤修复的作用机理。从而为加味白头翁汤应用于溃疡性结肠炎临床提供理论基础,同时对中医治则治法的现代化研究作有益探讨。
方法
将40只SPF级健康SD大鼠,雌雄各半,随机分为正常对照组、模型组、柳氮磺胺吡啶组、加味白头翁汤组,每组10只。采用三硝基苯磺酸([NBS)局部灌肠加高脂高糖法建立UC大鼠模型,动物模型制作成功后,中药治疗组给予加味白头翁汤灌胃,西药对照组给予柳氮磺胺吡啶(SASP)灌胃,模型组及正常对照组给予等容积的生理盐水灌胃,每天1次,连用15d。治疗结束后将大鼠固定于鼠解剖台上,腹腔注射20%氨基甲酸乙酯麻醉,剖取整个结肠组织,先行肉眼仔细观察各组大鼠结肠粘膜的充血、水肿、伪膜、溃疡和糜烂数目及面积病理改变情况,然后再取少量结肠粘膜组织石蜡包埋,HE染色,光镜观察大鼠结肠组织病理形态学变化。剩余结肠粘膜标本运用蛋白免疫印迹(Western blot)法检测NF-κB的蛋白表达水平,用Real-time PCR方法测定β-防御素-2、TFF3的基因表达变化,免疫组化法观察TGFβ1、EGF蛋白表达的变化。
结果
1加味白头翁汤方组与模型组相比较：大鼠的一般情况明显好转,大鼠脓血便和粘液便消失,大便成形,活动灵活,食欲好转,大鼠体重明显增高。加味白头翁汤方可使结肠粘膜组织损伤和病理组织学评分降低,与模型组比较,差异显著(P<0．01)。结肠粘膜组织的充血、水肿、伪膜、溃疡和糜烂数目及面积减少,肠壁损伤修复,炎性细胞浸润减少,溃疡附近肠粘膜可见不连续粘液层覆盖,而粘膜下层则可见胶原纤维增生。
2与正常组比较,模型组大鼠NF-KB p65表达显著增高,差异显著(P<0.01)；给予加味白头翁汤治疗后,NF-KB p65表达明显下降,与模型组比较,差异显著(P<0.01)；中药治疗组与西药对照组比较无显著差异(P>0.05)。
3与正常组比较,模型组大鼠结肠粘膜β-防御素-2表达显著增高,差异显著(P<0.01)；给予加味白头翁汤治疗后,结肠粘膜β-防御素-2基因表达明显下降,与模型组比较,差异显著(P<0.01),中药治疗组与西药对照组比较无显著差异(P>0.05)。
4与正常组比较,模型组大鼠结肠粘膜TFF3略有降低,但没有显著差异(P>0.05)；给予加味白头翁汤治疗后,结肠粘膜TFF3基因表达明显上升,与模型组比较,差异显著(P<0.01)；中药治疗组与西药对照组比较无显著差异(P>0.05)。
5与正常组比较,模型组TGF β1的表达明显增高,两组比较差异显著(P<0.01),给予加味白头翁汤治疗后,TGF β1相对表达明显下降,与模型组比较,差异显著(P<0.01),中药治疗组与西药对照组比较无显著差异(P>0.05)。与正常组比较,模型组EGF的表达明显低于正常组,两组比较差异显著(P<0.01)；给予加味白头翁汤治疗后,EGF蛋白相对表达明显增高,与模型组比较,差异显著(P<0.01),中药治疗组与西药对照组比较无显著差异(P>0.05)。
结论
1加味白头翁汤方可抑制UC的炎性细胞浸润,使炎症减轻,同时还有促进结肠粘膜损伤修复,恢复结肠粘膜的分泌功能的作用。说明本课题UC模型复制成功。加味白头翁汤方可通过减轻结肠炎症,促进结肠粘膜修复,从而起到治疗UC的作用。
2NF-KB p65的表达与UC病情严重性和活动性之间有一定关系,提示UC结肠粘膜组织的NF-KB表达水平可反映结肠组织的损害程度,对于病情评估和治疗效果判断可能具有潜在指导意义。加味白头翁汤组对UC大鼠模型过度激活的NF-KB有抑制作用,这可能是加味白头翁汤组治疗UC大鼠的作用机理之一。
3加味白头翁汤方的治疗作用可能在于通过下调β-防御素-2基因表达含量,进而减轻结肠粘膜的炎症反应,杀伤肠道病原微生物,起到粘膜修复的作用。β-防御素-2可能是加味白头翁汤治疗UC作用的关键的靶位。
4加味白头翁汤方可通过增加结肠上皮细胞TFF3的分泌从而促进受损结肠粘膜组织的修复。
5加味白头翁汤对UC大鼠模型结肠粘膜TGF β1蛋白表达有下调作用,从而抑制炎症的发生发展；对UC大鼠EGF的蛋白表达则有上调作用,能够促进受损粘膜周围的完好上皮细胞向损伤粘膜表面迁移覆盖,加快损伤粘膜的修复。
Objective
The etiology and pathogenesis of ulcerative colitis (UC) is not very clear. In recent years, with in-depth study of ulcerative colitis, the incidence and treatment of ulcerative colitis have a new understanding that regardless of the primary lesion of the intestinal tract, or consequential damages, would result in the colon closely related to the mucous membrane structure and function of injury in the pathogenesis of ulcerative colitis. Mucosa is not only an important place of nutrient digestion and absorption but also pathogenic microorganisms and toxins to invade the main portal.Under physiological conditions, the body through the mucosal barrier to effectively prevent the invasion of pathogenic microorganisms and toxins in order to ensure that the body in a healthy state. Microorganisms and toxins can break through the intestinal mucosal barrier into the portal vein and the lymphatic system. They also can cause bacterial translocationand the development of ulcerative colitis.
To explicit inflammatory cells regulating factor of NF-κB, β-defensin-2, TFF3,EGF and TGF-beta in intestinal self-protection and damage repair mechanisms, the subject of high-fat high-sugar diet plus TNBS enema copy ulcerative colitis rat model and tracking them back in the colonic mucosa damage, the study focused on the regulation ofinflammatory cell factor NF-κB transcription factor. In the intestinal repairing, the study focused on the β-defensin-2, TFF3and EGF and TGF-beta in the Ulcerative Colitis change and relatedregulation mechanism in the development and mucosal repair process. Through observation the Modified Pulsatilla Decoction on the NF-κB activation and β-defensin-2, TFF3and TGFβ1,EGF expression, and then explore the intestinal injury and repair mechanism of the Added Pulsatilla Decoction on ulcerative colitis, and to provide theoretical foundation on Added Pulsatilla Decoction used in ulcerative colitis clinical.
Methods
40of SPF health SD rats were randomly divided into normal control group, model group,the sulfasalazine group, Added Pulsatilla Decoction group.(N=10). Trinitrobenzene sulfonic acid (TNBS) local enema plus high fat and sugar established the UC rat model. After the success of produced Animal model,the treatment group given modified the Pulsatilla soup gavage, the comparison group given sulfasalazine (SASP) orally once a day, model group and normal control group given the same volume of of normal saline once a15d. After end of treatment, rats were fixed on the rat of dissecting table, the intraperitoneal injection of20%urethane anesthesia, dissected the entire colon tissue, first carefully observed by the naked eye the colonic mucosa of rats in each group congestion, edema, pseudomembranous, ulcers and erosions.The number and size of the pathological changes, and then take a small amount of colonic mucosa tissue embedded in paraffin, HE staining and observed by light microscopy, the pathological changes of rat colon tissue. The remaining colonic mucosa specimens using Western blot (Western blot analysis) assay of NF-κB protein expression levels, Real-time PCR method for determination of (3-defensins-2TFF3gene expression changes in the immunohistochemical method observation of TGFβ1and EGF changes in protein expression.
Results
1Compared with model group, the general situation in Added Pulsatilla Decoction group was significantly improved, in rat blood and pus and mucus disappeared, stool forming, flexible activities, improved appetite, body weight of rats was significantly higher. Added Pulsatilla Decoction group can make the intestine mucosal injury and histological score lower, compared with model group, the difference was significant (P<0.01). Intestine mucosal congestion, edema, pseudomembranous, ulcers, and erosion number and size were reduced, intestinal damage were repaired, inflammatory cell infiltration were reduced, ulcer mucosa can be seen near continuous mucus layer covering the submucosa visible collagen fibers.
2Compared with normal group, the model group rats of NF-KB of p65expression significantly with increased,(P<0.01); given to the treatment of Added Pulsatilla Decoction, NF-κB of p65expression was significantly decreased, compared with model group, the differences was significant (P <0.01); treatment group and comparison group showed no significant differences (P>0.05).
3Compared with normal group, model group rats colonic mucosa beta-defensin-2expression was significantly higher, the difference was significant (P<0.01); give Added Pulsatilla Decoction treatment, the colonic mucosa beta-defensin-2gene expression was significantly decreased. Compared with model group, the difference was significant (P<0.01), treatment group and comparison group showed no significant difference (P>0.05).
4Compared with the normal group, the model group rat colonic mucosa ITF decreased slightly, but no significant differences (P>0.05); given Added Pulsatilla Decoction treatment, the colonic mucosa TFF3gene expression increased significantly compared with the model group, the difference was significant (P<0.01); treatment group and comparison group showed no significant difference (P>0.05).
5Compared with the normal group, model group TGFβ1of expression was significantly increased, the differences was significant (P<0.01), to give Added Pulsatilla Decoction treatment of TGFβ1is relatively express the amount for the significantly decreased, compared with model group,the differences was significant (P<0.01), treatment group and western medicine in the control group showed no significant difference (P>0.05). Compared with the normal group, model group, EGF expression was significantly lower than the normal group, the difference was significant (P<0.01); give Added Pulsatilla Decoction treatment of EGF protein relative expression was significantly increased compared with model group, the difference was significant (P<0.01), treatment group and comparison group showed no significant difference (P>0.05).
Conclusion
1The Added Pulsatilla Decoction can inhibit the inflammatory cell infiltration of the UC, reduced the inflammation, as well as promote the repair of the colonic mucosa damage and restore the secretory function of the colonic mucosa. The model of UC were copied successfully. The Added Pulsatilla Decoction can reduce colonic inflammation, promote colonic mucosa repair, and thus play a role in the treatment of UC.
2Have a certain relationship between the NF-κB p65expression and UC disease severity and activity, suggesting that the organization of the UC colonic mucosa of NF-KBexpression level may reflect the extent of damage of the colon tissue, the judgment of the condition assessment and treatment effects may potentially guidance. The Added Pulsatilla Decoction can inhibit the excessive activation of NF-KB on UC rat model, which may be one of the mechanisms of the Added Pulsatilla Decoction group on the treatment of UC rats.
3The Added Pulsatilla Decoction of therapeutic effect may be that the content by down-regulating β-defensin-2gene expression, and thus reduce the inflammation of thecolonic mucosa, destruction of intestinal pathogenic microorganisms, play a role inmucosal repair. beta-defensin-2may be the role of key target by Added Pulsatilla Decoction treatment of UC
4The Added Pulsatilla Decoction can increase the TFF3secretion in the colonic epithelial cells and to promote tissue repair of the damaged colonic mucosa.
5The Added Pulsatilla Decoction can downward TGF(31protein expression of the UC rat,and inhibit the inflammation development. The Added Pulsatilla Decoction can increase the EGF protein expression of UC rat, can contribute to the damaged mucous membrane surrounding the integrity of the epithelial cells to injury the migration of the mucosal surface coverage, accelerate the repair of damaged mucosa.
引文
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