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目的观察冷束缚应激(coldrestrainstress,CRS)状态下大鼠小肠黏膜细胞的凋亡情况;探讨CRS状态下对大鼠小肠黏膜细胞凋亡的影响机制。方法选取出生80~100d的SD大鼠为实验动物,随机分为正常对照组(N组)和冷束缚应激组(S组),S组按应激后检测时间又分为S2h、S4h、S8h、S12h、S24h组,应激动物模型制作参照Brodie的方法制作。分别观察各组大鼠的小肠黏膜细胞凋亡情况,以原位末端标记法(TUNEL)法检测2组小肠黏膜细胞凋亡情况;免疫组化法检测bcl-2以及PCNA的表达情况。结果S组中各时段组大鼠小肠黏膜细胞凋亡率明显高于N组(除24h组隐窝外)。2h、4h、8h组未见bcl-2的表达,N组和S12h、S24h组可见少量表达。而2组的PCNA的表达情况无明显差异。结论应激状态下小肠黏膜细胞凋亡明显增加,从而导致肠屏功能的损伤,而在短期内对小肠黏膜细胞增殖无明显影响。
Objective To observe the apoptosis of rat intestinal mucosa under cold stress condition (CRS) and to explore the mechanism of the effect of CRS on the apoptosis of rat intestinal mucosa. Methods SD rats 80 days old and 80 days old were selected as experimental animals and randomly divided into normal control group (N group) and cold restraint stress group (S group). S group was divided into S2h, S4h, S8h, S12h, S24h group, stress animal model making reference to Brodie’s method. The apoptosis of small intestinal mucosal cells in each group was observed. The apoptosis of intestinal mucosa in 2 groups was detected by TUNEL method. The expressions of bcl-2 and PCNA were detected by immunohistochemistry. Results The apoptotic rates of small intestinal mucosa of rats in S group were significantly higher than those in N group (except the crypts of 24h group). No expression of bcl-2 was observed in 2h, 4h, 8h group, and a small amount of expression was observed in group N, S12h and S24h. The expression of PCNA in the two groups had no significant difference. Conclusion The apoptosis of small intestinal mucosa significantly increased under stress, which led to the damage of intestinal function, but had no significant effect on the proliferation of small intestinal mucosa in a short time.