| Ulcerative colitis (UC), a non-specific chronic inflammatory, primarily involves in the mucosa and submucosa of rectum and colon. It is characterized by the ulceration. But the cause of UC is still unknown. Diarrhea, bloody purulent stool, abdominal pain and tenesmus are the clinical features of UC. It is considered previously that UC was common in Europe and America and was less common in Asian and African. However the study shows UC is also common in China in recent decades. As UC occurs slowly and repeatedly, has a long course, and be easy to develop into cancer, so it has an unbeneficial effect on patient's life. UC has been regarded as one of the modern refractory diseases by WHO.At present, the kind of aminosalicylic acid and corticoid are used to treat this disease. But these drugs could cause much adverse reaction to people. Traditional Chinese medicine (TCM) show advantages in syndrome differentiation and regulating body from the whole. It has abundant clinical practice, so it is worthy of research. Wumei Wan is a classical prescription that could be used to treat chronic diarrhea. Jiawei Wumei Wan (JWW) was composed of many herbs guided by TCM theory, clinical experiences, and technological research findings. The investigation aimed to observe the protective role of JWW to UC rats induced by TNBS. This study includes literature review, prescription analysis, the function of JWW to experimental UC and its mechanism exploration.1. Literature reviewWe had reviewed literatures about the general situation of UC from TCM and western medicine in domestic and abroad.2. The demonstration of Jiawei Wumei WanJWW that guided by TCM theories, clinical experiences, and technological research findings is demonstrated.3. The protective effect of JWW to UC induced by TNBSRats were divided into six groups randomly, which includes normal group, model group, SASP group and JWWW high-dose, middle-dose, low-dose group. The UC rats were induced by TNBS/ethanol through enema. Normal group and model group was given distilled water through mouth in 1ml/(100g·d) for two weeks. SASP group was given SASP through mouth in 0.5g/kg for two weeks. JWWW groups were given oral liquid through mouth respectively in 22.17g/kg, 11.08g/kg and 5.54g/kg.A disease activity index (DAI) was determined by scoring the extent of body weight loss, stool consistency and stool haemoccult positivity or gross bleeding. The result was that DAIs were lower in the rats treated with JWW than that of the model group (P＜0.05). The data indicated that the model was successful. JWW could suppress the damage, interrupt UC.After 14 days' treatment, taken the colon out, observed the length, the max width, colon mucosa damage index and histological score. Compared with the model group, JWW could enhance the max width, but has no influence to the length. JWW could lower the histological score and significantly inhibited the colon mucosa damage index. The finding further suggested the model was successful. JWW has the treatment function to UC induced by TNBS through diminishing inflammation of colon, promoting the repairment of mucosa and recovering the secretion of colon.Myeloperoxidase (MPO) in pathological colon tissue was measured. The result showed JWW could suppress content of MPO.4. Mechanism explorationsInspect the content of IL-6 and TNF-αin serum of UC in rats, it showed that JWW could down-regulate their level.Apoptosis of the lymphocyte was detected by the technique of TUNEL. The positive cells were yellow. Apoptosis of lymphocytes were decreased in JWW groups compared with model group. JWW showed to exert treatment function on the mucosa in UC possibly by promoting apoptosis of lymphocytes in lamina propria.The expression of NF-κB p65 was determined by immunohistochemistry. The positive cells were yellow. NF-κB was expressed negatively or weakly in normal group. The positive cells of model group were mainly expressed in mononuclearcells and epithelial cells of crypt, enterocyte had a few expression. Most positive cells were mostly localized in the nucleus of cells, while little in the cytoplasm. The expression of NF-κB was lower in JWW than that of model group. The investigation implicated that JWW exerted the treatment function by blocking activity of NF-κB.5. ConclusionsIn conclusion, JWW exerted the treatment function by inhibiting TNF-α, thus suppressing the activity of NF-κB, and then causing the decreace of IL and TNF-αexpression, promoting apoptosis of lymphocytes under the regulation of NF-κB and TNF-α. |
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