DEGRADED CARRAGEENAN-INDUCED COLITIS IN CF1 MICE - A CLINICAL, HISTOPATHOLOGICAL AND KINETIC-ANALYSIS
DEGRADED CARRAGEENAN-INDUCED COLITIS IN CF1 MICE - A CLINICAL, HISTOPATHOLOGICAL AND KINETIC-ANALYSIS
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DOI：
10.1159/000199033
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发表时间：
1984-01-01
期刊：
影响因子：
3.2
通讯作者：
DWORKIN, BM
中科院分区：
文献类型：
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作者：
FATH, RB;DESCHNER, EE;DWORKIN, BM
将10%角叉菜胶（降解的角叉菜胶）在饮用水中递送给CF 1小鼠10天，诱导血性腹泻、隐周炎症和盲肠和升结肠的显著扩张。在组织学上，粘膜的特征在于变形的隐窝结构、固有层的炎性浸润和溃疡，这些情况在近端结肠中更明显，但也存在于远端结肠中。用氢化可的松和左旋咪唑处理降低了反应所有阶段的严重程度。结肠上皮细胞增殖的改变与临床和组织病理学结果一致。标记指数（LI）在两个近端（12.9 ± 0.01）显著高于对照值。4.9 vs. 7.6 .+-。2.9)和远端结肠（13.9 ±. 5.2 vs. 7.2 .+-。2.4），有效地使两个区域中每个隐窝柱的增殖细胞数加倍。然而，DNA合成细胞沿着近端结肠的隐窝壁进一步向上延伸，反映了更大的粘膜损伤。仅在近端结肠中，增殖区室（PC）延伸到腺体的上三分之一，通常不是增殖区。氢化可的松和左旋咪唑与10%角叉菜胶同时给药在保护近端结肠方面效果较差，因为远端结肠中LI和每个隐窝柱的标记细胞数始终较低。此外，氢化可的松单独显着抑制DNA合成仅在远端结肠。所有远端结肠隐窝没有同样的保护，因为一些继续表达大量的增殖细胞和扩展的PC，以及表征癌前缺陷的结肠上皮细胞增殖的调节控制氢化可的松的管理。角叉菜胶诱导的小鼠结肠炎的临床表现、组织病理学、增殖性改变、潜在的癌前病变和对药物干预的反应支持其作为人类溃疡性结肠炎动物模型的继续研究。
Delivery of 10% carrageen (degraded carrageenan) for 10 days in the drinking water to CF1 mice induced bloody diarrhea, pericryptal inflammation and marked dilatation of the cecum and ascending colon. Histologically, the mucosa was characterized by distorted crypt architecture, inflammatory infiltration of the lamina propria and ulceration, conditions which were more pronounced in the proximal colon but were also present in the distal colon. treatment with hydrocortisone and levamisole reduced the severity of all phases of the reaction. Alterations in colonic epithelial cell proliferation corresponded with the clinical and histopathological findings. Labeling indices (LI) significantly increased over control values in both proximal (12.9 .+-. 4.9 vs. 7.6 .+-. 2.9) and distal colon (13.9 .+-. 5.2 vs. 7.2 .+-. 2.4), effectively doubling the number of proliferating cells per crypt column in both areas. However, DNA-synthesizing cells extended further upward along the cryptal wall of the proximal colon reflecting greater mucosal damage. Only in the proximal colon did the proliferative compartment (PC) extend to the upper third of the glands, normally not a proliferative zone. Hydrocortisone and levamisole administered concurrently with 10% carrageen were less effective in protecting the proximal colon since LI and numbers of labeled cells per crypt column were consistently lower in the distal colon. Moreover, hydrocortisone alone significantly depressed DNA synthesis only in the distal colon. All distal colonic crypts were not equally protected by administration of hydrocortisone since some continued to express large numbers of proliferating cells and an extended PC, well characterized preneoplastic defects in regulatory control of colonic epithelial cell proliferation. The clinical presentation, histopathology, proliferative alterations, potential premalignancy and response to pharmaceutic intervention of carrageen-induced colitis in mice support its continued investigation as an animal model for human ulcerative colitis.