摘要
Objective: To discuss the changes in the tight junction protein of intestinal epithelium and permeability of colonic mucosa and its possible mechanism by building the rat mode of inflammatory bowel disease at the chronic recovery stage. Methods: A total of 36 SD rats were divided into the model group and control one according to the random number table, with 18 rats in each group. Rats in the model group were given the 3% dextran sulfate sodium solution by the way of drinking for 7 d to build the rat model of inflammatory bowel disease, while rats in the control group were given free drinking of water. Six rats were executed at day 7, 14 and 21 respectively. The colonic tissues were collected from rats to observe the pathological changes of colonic mucosa. The activity of myeloperoxidase was detected and the white blood count was performed for rats in each group. The Ussing chamber technique was employed to detect the transepithelial electrical resistance(TER) and short-circuit current(SC) of colonic mucosa of rats in different time intervals; the quantum dots labeling technique was employed to detect the expression level of claudin-1 and claudin-2 in the colonic tissues. Results: After the successful modeling, the weight of rats in the model group was significantly reduced, while the disease activity index score was increased. The weight was at the lowest level at day 14 and then it began to increase afterwards. The disease activity index score was at the highest level at day 12 and then it began to decrease gradually. The activity of myeloperoxidase and WBC for rats in the model group all reached the peak value at day 14 and then decreased gradually. There was no significant difference in the changes of TER and SC in different time intervals for rats in the control group(P>0.05). TER of model group was at the lowest level at day 14 and then increased gradually; SC was at the highest level at day 14 and then decreased gradually. TER of model group at day 7, 14 and 21 was significantly lower than that of control
Objective: To discuss the changes in the tight junction protein of intestinal epithelium and permeability of colonic mucosa and its possible mechanism by building the rat mode of inflammatory bowel disease at the chronic recovery stage. Methods: A total of 36 SD rats were divided into the model group and control one according to the random number table, with 18 rats in each group. Rats in the model group were given the 3% dextran sulfate sodium solution by the way of drinking for 7 d to build the rat model of inflammatory bowel disease, while rats in the control group were given free drinking of water. Six rats were executed at day 7, 14 and 21 respectively. The colonic tissues were collected from rats to observe the pathological changes of colonic mucosa. The activity of myeloperoxidase was detected and the white blood count was performed for rats in each group. The Ussing chamber technique was employed to detect the transepithelial electrical resistance (TER) and short-circuit current (SC) of colonic mucosa of rats in different time intervals; the quantum dots labeling technique was employed to detect the expression level of claudin-1 and claudin-2 in the colonic tissues. Results: After the successful modeling, the weight of rats in the model group was significantly reduced, while the disease activity index score was increased. The weight was at the lowest level at day 14 and then it began to increase afterwards. The disease activity index score was at the highest level at day 12 and then it began to decrease gradually. The activity of myeloperoxidase and WBC for rats in the model group all reached the peak value at day 14 and then decreased gradually. There was no significant difference in the changes of TER and SC in different time intervals for rats in the control group (P>0.05). TER of model group was at the lowest level at day 14 and then increased gradually; SC was at the highest level at day 14 and then decreased gradually. TER of model group at day 7, 14 and 21 was significantly lower than that of contr
基金
supported by Project of Science and Technology Development of Hubei Province(No.2013HBF21825)
