目的:探讨还原型巨噬细胞诱导剂N-乙酰半胱氨酸(N-Acetylcysteine,NAC)对硫酸葡聚糖钠(Dextran Sodi- um Sulphate,DSS)诱导的小鼠实验性肠炎的预防及治疗作用。方法:建立DSS实验性小鼠肠炎模型,NAC及氧化型巨噬细胞诱导剂N,N’-联乙(?)...目的:探讨还原型巨噬细胞诱导剂N-乙酰半胱氨酸(N-Acetylcysteine,NAC)对硫酸葡聚糖钠(Dextran Sodi- um Sulphate,DSS)诱导的小鼠实验性肠炎的预防及治疗作用。方法:建立DSS实验性小鼠肠炎模型,NAC及氧化型巨噬细胞诱导剂N,N’-联乙(?)-L-胱氨酸(N,N’-diacetyle-L-cystine,(NACOMe)2)在致模前后腹腔注射;检测腹腔巨噬细胞中还原型谷胱甘肽(GSH)与氧化型谷胱甘肽(GSSG)的变化;对结肠进行病理学评价,并检测结肠IL-4、IFN-g的表达。结果:NAC预处理组:结肠长度和病理学指标均优于其他预处理组,腹腔巨噬细胞内GSH及GSH/GSSG升高;结肠分泌的IL-4、IFN-γ明显降低。NAC治疗组:体重增加程度明显高于其它治疗组,结肠炎症及黏膜损伤较轻,腹腔巨噬细胞内GSSG明显减低,GSH和GSH/GSSG升高,病变结肠分泌的IL-4、IFN-γ明显降低。结论:还原型巨噬细胞诱导剂NAC可以通过诱导巨噬细胞内GSH产生增多从而减轻实验性肠炎的黏膜损伤及临床症状,对DSS诱导的实验性肠炎有一定的预防及治疗作用。展开更多
微量元素硒对炎性肠道疾病的免疫调控效应一直是研究关注的焦点.本文采用葡聚糖硫酸钠诱导的实验性小鼠急性溃疡性结肠炎模型,观察了亚硒酸钠(Na_(2)SeO_(3))灌胃对肠道局部及相关淋巴组织中的天然免疫细胞、适应性免疫B细胞、细胞毒性...微量元素硒对炎性肠道疾病的免疫调控效应一直是研究关注的焦点.本文采用葡聚糖硫酸钠诱导的实验性小鼠急性溃疡性结肠炎模型,观察了亚硒酸钠(Na_(2)SeO_(3))灌胃对肠道局部及相关淋巴组织中的天然免疫细胞、适应性免疫B细胞、细胞毒性T细胞(cytotoxic T cells,CTL)和辅助性T细胞(helper T cells,T_(H))的不同亚群T_(H)1,T_(H)2,调节性T细胞(regulatory T cells,T_(reg))及滤泡辅助性T细胞(follicular helper T cells,T_(FH))等的功能分化调控效应,并在体外观察了Na_(2)SeO_(3)对T_(FH)细胞分化的调控规律.结果显示,亚硒酸钠灌胃补硒可以加重急性肠炎,并促进T_(FH)细胞在肠道局部及肠周围淋巴组织浸润和B细胞免疫球蛋白A(immunoglobulin A,IgA)分泌.这为微量元素硒免疫调控肠道炎性疾病研究提供了依据,也为硒的临床应用研究提供了实验数据.展开更多
AIM： To evaluate the therapeutic effects of a probiotic supplement （Clostridium butyricum, CGMCC0313 ） in a chemically-induced rat model of experimental colitis. METHODS： An experimental ulcerative colitis model w...AIM： To evaluate the therapeutic effects of a probiotic supplement （Clostridium butyricum, CGMCC0313 ） in a chemically-induced rat model of experimental colitis. METHODS： An experimental ulcerative colitis model was established by rectal injection of oxazolone into the colon of 40 Wistar rats randomly divided into four groups. The positive control group was sacrificed 3 d after colitis onset. The remaining groups were fed daily with either 2 mL of C. butyricum （2.3 × 10^11 CFU/L）, 2 mL of mesalamine （100 g/L）, or 1 mL of sodium butyrate （50 mmol/L） for 21 d. The animals＇ body weight, behavior, and bowel movements were recorded weekly. After sacrifice, visual and microscopic observations of pathological changes of colon tissue were made, body weight and wet colon mass index were measured and recorded, and serum levels of interleukin-23 （IL-23） and TNF-α were measured using ELISA. Expression of calcitonin gene-related peptide in colon tissue was measured by RT-PCR. Finally, changes in rat intestinal microflora status were measured in all groups.lowered the serum levels of both IL-23 and tumor necrosis factor-α （TNF-α） with similar or even better efficiency than that of mesalamine or sodium butyrate. The rat intestinal flora appeared to recover more quickly in the group treated with C. butyricum than in the mesalamine and sodium butyrate groups. Finally, we found that the expression level of calcitonin gene related peptide was elevated in colon tissue in the sodium butyrate treated group but not in the C. butyricum or mesalamine treated groups, indicating a sensitization of colon following sodium butyrate treatment. CONCLUSION： In our experimental colitis model, treatment with C. butyricum CGMCC0313, a probiotic supplement, is at least as efficient as treatment with mesalamine.展开更多
文摘目的:探讨还原型巨噬细胞诱导剂N-乙酰半胱氨酸(N-Acetylcysteine,NAC)对硫酸葡聚糖钠(Dextran Sodi- um Sulphate,DSS)诱导的小鼠实验性肠炎的预防及治疗作用。方法:建立DSS实验性小鼠肠炎模型,NAC及氧化型巨噬细胞诱导剂N,N’-联乙(?)-L-胱氨酸(N,N’-diacetyle-L-cystine,(NACOMe)2)在致模前后腹腔注射;检测腹腔巨噬细胞中还原型谷胱甘肽(GSH)与氧化型谷胱甘肽(GSSG)的变化;对结肠进行病理学评价,并检测结肠IL-4、IFN-g的表达。结果:NAC预处理组:结肠长度和病理学指标均优于其他预处理组,腹腔巨噬细胞内GSH及GSH/GSSG升高;结肠分泌的IL-4、IFN-γ明显降低。NAC治疗组:体重增加程度明显高于其它治疗组,结肠炎症及黏膜损伤较轻,腹腔巨噬细胞内GSSG明显减低,GSH和GSH/GSSG升高,病变结肠分泌的IL-4、IFN-γ明显降低。结论:还原型巨噬细胞诱导剂NAC可以通过诱导巨噬细胞内GSH产生增多从而减轻实验性肠炎的黏膜损伤及临床症状,对DSS诱导的实验性肠炎有一定的预防及治疗作用。
文摘微量元素硒对炎性肠道疾病的免疫调控效应一直是研究关注的焦点.本文采用葡聚糖硫酸钠诱导的实验性小鼠急性溃疡性结肠炎模型,观察了亚硒酸钠(Na_(2)SeO_(3))灌胃对肠道局部及相关淋巴组织中的天然免疫细胞、适应性免疫B细胞、细胞毒性T细胞(cytotoxic T cells,CTL)和辅助性T细胞(helper T cells,T_(H))的不同亚群T_(H)1,T_(H)2,调节性T细胞(regulatory T cells,T_(reg))及滤泡辅助性T细胞(follicular helper T cells,T_(FH))等的功能分化调控效应,并在体外观察了Na_(2)SeO_(3)对T_(FH)细胞分化的调控规律.结果显示,亚硒酸钠灌胃补硒可以加重急性肠炎,并促进T_(FH)细胞在肠道局部及肠周围淋巴组织浸润和B细胞免疫球蛋白A(immunoglobulin A,IgA)分泌.这为微量元素硒免疫调控肠道炎性疾病研究提供了依据,也为硒的临床应用研究提供了实验数据.
基金The Model Subject of High-Tech Industrializing Conversion of Series Microecological New Drugs,National Development and Reform Commission High-Tech,[2004]2078
文摘AIM： To evaluate the therapeutic effects of a probiotic supplement （Clostridium butyricum, CGMCC0313 ） in a chemically-induced rat model of experimental colitis. METHODS： An experimental ulcerative colitis model was established by rectal injection of oxazolone into the colon of 40 Wistar rats randomly divided into four groups. The positive control group was sacrificed 3 d after colitis onset. The remaining groups were fed daily with either 2 mL of C. butyricum （2.3 × 10^11 CFU/L）, 2 mL of mesalamine （100 g/L）, or 1 mL of sodium butyrate （50 mmol/L） for 21 d. The animals＇ body weight, behavior, and bowel movements were recorded weekly. After sacrifice, visual and microscopic observations of pathological changes of colon tissue were made, body weight and wet colon mass index were measured and recorded, and serum levels of interleukin-23 （IL-23） and TNF-α were measured using ELISA. Expression of calcitonin gene-related peptide in colon tissue was measured by RT-PCR. Finally, changes in rat intestinal microflora status were measured in all groups.lowered the serum levels of both IL-23 and tumor necrosis factor-α （TNF-α） with similar or even better efficiency than that of mesalamine or sodium butyrate. The rat intestinal flora appeared to recover more quickly in the group treated with C. butyricum than in the mesalamine and sodium butyrate groups. Finally, we found that the expression level of calcitonin gene related peptide was elevated in colon tissue in the sodium butyrate treated group but not in the C. butyricum or mesalamine treated groups, indicating a sensitization of colon following sodium butyrate treatment. CONCLUSION： In our experimental colitis model, treatment with C. butyricum CGMCC0313, a probiotic supplement, is at least as efficient as treatment with mesalamine.
