临床儿科杂志
臨床兒科雜誌
림상인과잡지
2013年
10期
953-958
,共6页
刘俊红%吴斌%赖乾坤%林春
劉俊紅%吳斌%賴乾坤%林春
류준홍%오빈%뢰건곤%림춘
食物过敏%卵白蛋白%大鼠
食物過敏%卵白蛋白%大鼠
식물과민%란백단백%대서
food allergy%ovalbumin%rat
目的：探讨采用卵白蛋白（OVA）低剂量腹腔注射基础致敏及高剂量灌胃激发建立SD幼鼠食物过敏模型的适宜条件，并对模型进行评价。方法16只3周龄的雌性SD幼鼠随机分为过敏组和对照组，每组8只。实验第1天过敏组予腹腔注射OVA 40μg和氢氧化铝混悬液0.2 ml（氢氧化铝1 mg），第2、4、7、9、11天腹腔注射OVA 0.2 ml（40μg）进行基础致敏；第20、24、28、30天予OVA 2.0 ml（15 mg/ml）灌胃激发；对照组同期给予同等容量的生理盐水腹腔注射和灌胃。观察两组幼鼠肠黏膜嗜酸性粒细胞和肥大细胞密度、肥大细胞完整率及血清OVA-IgE含量变化。结果与对照组相比，过敏组幼鼠毛发无光、排稀便，血清OVA-IgE明显升高，差异有统计学意义（P<0.01）；过敏组幼鼠空肠、回肠、结肠肠黏膜损伤，嗜酸性粒细胞浸润明显，肥大细胞聚集伴脱颗粒数目增多，差异有统计学意义（P<0.01）。结论采用致敏原OVA与免疫佐剂氢氧化铝，通过低剂量腹腔注射致敏联合高剂量灌胃激发所诱导的幼鼠模型与婴幼儿食物过敏临床特征、肠道病理改变一致，是一种理想的SD幼鼠食物过敏模型。
目的：探討採用卵白蛋白（OVA）低劑量腹腔註射基礎緻敏及高劑量灌胃激髮建立SD幼鼠食物過敏模型的適宜條件，併對模型進行評價。方法16隻3週齡的雌性SD幼鼠隨機分為過敏組和對照組，每組8隻。實驗第1天過敏組予腹腔註射OVA 40μg和氫氧化鋁混懸液0.2 ml（氫氧化鋁1 mg），第2、4、7、9、11天腹腔註射OVA 0.2 ml（40μg）進行基礎緻敏；第20、24、28、30天予OVA 2.0 ml（15 mg/ml）灌胃激髮；對照組同期給予同等容量的生理鹽水腹腔註射和灌胃。觀察兩組幼鼠腸黏膜嗜痠性粒細胞和肥大細胞密度、肥大細胞完整率及血清OVA-IgE含量變化。結果與對照組相比，過敏組幼鼠毛髮無光、排稀便，血清OVA-IgE明顯升高，差異有統計學意義（P<0.01）；過敏組幼鼠空腸、迴腸、結腸腸黏膜損傷，嗜痠性粒細胞浸潤明顯，肥大細胞聚集伴脫顆粒數目增多，差異有統計學意義（P<0.01）。結論採用緻敏原OVA與免疫佐劑氫氧化鋁，通過低劑量腹腔註射緻敏聯閤高劑量灌胃激髮所誘導的幼鼠模型與嬰幼兒食物過敏臨床特徵、腸道病理改變一緻，是一種理想的SD幼鼠食物過敏模型。
목적：탐토채용란백단백（OVA）저제량복강주사기출치민급고제량관위격발건립SD유서식물과민모형적괄의조건，병대모형진행평개。방법16지3주령적자성SD유서수궤분위과민조화대조조，매조8지。실험제1천과민조여복강주사OVA 40μg화경양화려혼현액0.2 ml（경양화려1 mg），제2、4、7、9、11천복강주사OVA 0.2 ml（40μg）진행기출치민；제20、24、28、30천여OVA 2.0 ml（15 mg/ml）관위격발；대조조동기급여동등용량적생리염수복강주사화관위。관찰량조유서장점막기산성립세포화비대세포밀도、비대세포완정솔급혈청OVA-IgE함량변화。결과여대조조상비，과민조유서모발무광、배희편，혈청OVA-IgE명현승고，차이유통계학의의（P<0.01）；과민조유서공장、회장、결장장점막손상，기산성립세포침윤명현，비대세포취집반탈과립수목증다，차이유통계학의의（P<0.01）。결론채용치민원OVA여면역좌제경양화려，통과저제량복강주사치민연합고제량관위격발소유도적유서모형여영유인식물과민림상특정、장도병리개변일치，시일충이상적SD유서식물과민모형。
Objectives To explore suitable conditions for establishing food allergy model through sensitization by in-traperitoneal injection (i.p) with low-dose ovalbumin (OVA) and challenge by gavage with high-dose OVA in SD young rats, and to evaluate the model. Methods Sixteen three-week-old female SD young rats were randomly divided into two groups with 8 rats each. SD young rats in food allergy (FA) group were ifrst sensitized by intraperitoneal injection with 0.2 ml suspension mixed with 40 μg OVA and 1mg Al(OH)3 on the ifrst day (d 0), then intraperitoneally injected with 0.2 ml (40 μg) OVA solution on days 2, 4, 7, 9 and 11, and lastly challenged by gavage with 2.0 ml (15 mg/ml) OVA solution on days 20, 24, 28 and 30. The rats in the control group were intraperitoneally injected and gavaged with the same volume of normal saline instead of OVA during the same period. The eosinophils (EOS), mast cells (MC), the integrity of MC in intestinal mucosa of two groups were observed, and ovalbumin speciifc IgE (OVA-IgE) levels in serum were analyzed. Results The rats in FA group had lusterless hair and diarrhea, and compared with control group, OVA-IgE levels were increased signiifcantly (P<0.05). Compared with control group, the intestinal mucosa of jejunum, ileum and colon in FA group had more damage, with more EOS and degranu-lated MC aggregated (P<0.01). Conclusions The allergy model established through sensitization by intraperitoneal injection with low-dose OVA mixed with adjuvant Al(OH)3 and challenge by gavage with high-dose OVA in young rats had clinical features and intestinal pathological changes consistent with food allergy infants and it was an ideal food allergy model in SD young rats.
