CAJ | 학술논문

实验动物%消化系统损伤模型%复方血竭%2,4,6-三硝基苯磺酸%结肠炎%树突状细胞%Tol 样受体4%核因子κB%流式细胞仪%大鼠%免疫组织化学%RT-PCR%病理%北京市自然科学基金實驗動物%消化繫統損傷模型%複方血竭%2,4,6-三硝基苯磺痠%結腸炎%樹突狀細胞%Tol 樣受體4%覈因子κB%流式細胞儀%大鼠%免疫組織化學%RT-PCR%病理%北京市自然科學基金
실험동물%소화계통손상모형%복방혈갈%2,4,6-삼초기분광산%결장염%수돌상세포%Tol 양수체4%핵인자κB%류식세포의%대서%면역조직화학%RT-PCR%병리%북경시자연과학기금
Tissue Engineering%Colitis%Trinitrobenzenesulfonic Acid%Mesentery

背景：树突状细胞可调节肠道内环境的免疫反应，这一功能缺陷会导致炎症性肠病，Tol 样受体4/核因子κB通路与上述反应密切相关。目的：构建实验性结肠炎模型大鼠，观察复方血竭对其树突状细胞及Tol 样受体4/核因子κB 表达的影响并探讨其作用机制。 <br>　　方法：将大鼠随机抽样法分为空白对照组、模型组、复方血竭组和5-氨基水杨酸治疗组。除空白对照组外，其他3组大鼠建立2，4，6-三硝基苯磺酸诱导的实验性结肠炎模型。造模成功后，复方血竭组和5-氨基水杨酸治疗组分别给予复方血竭[0.75 g/(kg · d)]和5-氨基水杨酸[(100 mg/(kg·d)]灌胃治疗10 d。 <br>　　结果与结论：复方血竭组较模型组大鼠的疾病活动指数评分、大体形态损伤评分、病理组织学评分均显著降低(P <0.05)，5-氨基水杨酸治疗组、复方血竭组的症状、结肠组织损害均较模型组明显减轻。模型组大鼠肠系膜淋巴结CD80和CD86的表达率，Tol 样受体4，核因子κB 表达较其他3组均显著升高(P<0.05或P<0.01)。复方血竭组Tol 样受体4及核因子κB表达明显低于5-氨基水杨酸治疗组。结果证实，复方血竭可部分缓解实验性结肠炎模型大鼠的症状，有效抑制其肠系膜淋巴结中树突状细胞的活化。复方血竭可能通过抑制大鼠肠黏膜细胞Tol 样受体4和核因子κB的表达而缓解肠道的炎症反应。
배경：수돌상세포가조절장도내배경적면역반응，저일공능결함회도치염증성장병，Tol 양수체4/핵인자κB통로여상술반응밀절상관。목적：구건실험성결장염모형대서，관찰복방혈갈대기수돌상세포급Tol 양수체4/핵인자κB 표체적영향병탐토기작용궤제。 <br>　　방법：장대서수궤추양법분위공백대조조、모형조、복방혈갈조화5-안기수양산치료조。제공백대조조외，기타3조대서건립2，4，6-삼초기분광산유도적실험성결장염모형。조모성공후，복방혈갈조화5-안기수양산치료조분별급여복방혈갈[0.75 g/(kg · d)]화5-안기수양산[(100 mg/(kg·d)]관위치료10 d。 <br>　　결과여결론：복방혈갈조교모형조대서적질병활동지수평분、대체형태손상평분、병리조직학평분균현저강저(P <0.05)，5-안기수양산치료조、복방혈갈조적증상、결장조직손해균교모형조명현감경。모형조대서장계막림파결CD80화CD86적표체솔，Tol 양수체4，핵인자κB 표체교기타3조균현저승고(P<0.05혹P<0.01)。복방혈갈조Tol 양수체4급핵인자κB표체명현저우5-안기수양산치료조。결과증실，복방혈갈가부분완해실험성결장염모형대서적증상，유효억제기장계막림파결중수돌상세포적활화。복방혈갈가능통과억제대서장점막세포Tol 양수체4화핵인자κB적표체이완해장도적염증반응。
BACKGROUND:Dendritic cel s can regulate the immunological reaction in the intestinal tract, this functional deficit may induce inflammatory bowel disease. Tol-like receptor-4/nuclear factor-κB pathway is highly involved in this reaction. OBJECTIVE:To establish experimental colitis model in rats, to observe effects of resina draconis on dendritic cel s and Tol-like receptor-4/nuclear factor-κB expression in rats with experimental colitis, and to explore its action mechanism. METHODS:A total of 44 male Sprague-Dawley rats were randomly assigned to four groups (n=11):blank control group, model group, resina draconis group, 5-aminosalicylic acid treatment group. With the exception of blank control group, 2,4,6-trinitrobenzenesulfonic acid-induced ulcerative colitis models were established in the model group, resina draconis group and 5-aminosalicylic acid treatment group. After the models were successful y established, the rats in the resina draconis and 5-aminosalicylic acid treatment groups were intragastrical y treated with resina draconis [(0.75 g(kg·d)] and 5-aminosalicylic acid [100 mg(kg·d)] respectively for 10 days. RESULTS AND CONCLUSION:Disease activity index, macroscopic colonic damage score and histopathological score were significantly decreased in the resina draconis group compared with the model group (P<0.05). Symptoms and tissue damages were obviously lessened in the 5-aminosalicylic acid treatment and resina draconis groups compared with the model group. Expression rates of CD80 and CD86, as wel as expression levels of Tol-like receptor-4 and nuclear factor-κB were significantly higher in the model group compared with the blank control group, resina draconis group and 5-aminosalicylic acid treatment group (P<0.05, P<0.01). Tol-like receptor-4 and nuclear factor-κB expression was significantly lower in the resina draconis group than that in the 5-aminosalicylic acid treatment group. Experimental findings indicate that, resina draconis can partial y relieve experimental colitis symptoms in rats and effectively inhibit the activation of dendritic cel s in the mesenteric lymph node. Resina draconis can relieve enteric inflammatory reaction by suppressing the expression of Tol-like receptor-4 and nuclear factor-κB in rats.