急性坏死型胰腺炎大鼠肠粘膜CD44 mRNA的表达及生长激素的作用

目的 观察急性坏死型胰腺炎（ANP）大鼠肠粘膜CD44 mRNA表达、并探讨其与肠粘膜T淋巴细胞亚群和病理形态学变化的关系及生长激素（GH）的作用。方法 SD大鼠54只，随机分为3组：假手术组（SO）；ANP组；ANP＋GH组（0．75U／kg体重）。大鼠胰胆管内逆行推注5％牛磺胆酸钠溶液（1ml/kg体重）制备ANP模型。术后6、12、24h分批处死。逆转录聚合酶链反应研究CD44 mRNA的表达。免疫组织化学观察肠粘膜T淋巴细胞亚群。结果 ANP组各时点CD44 mRNA表达较SO组显著降低（P＜0．05）。GH上调CD44 mRNA的表达。ANP组术后6、12、24h肠粘膜CD3、CD4、CD8细胞数较SO组显著减少（P＜0．05），而GH治疗组肠粘膜CD3、CD4、CD8细胞数与SO组差异无差异性（P＞0．05）。ANP组肠上皮破损明显，GH治疗组肠粘膜结构基本完整。结论 ANP大鼠肠粘膜CD44 mRNA表达降低，而GH维持肠粘膜上皮结构完整及粘膜免疫功能的作用可能与上调CD44 mRNA表达有关。

CD44 mRNA expression in intestinal mucosa of rats after acute necrotizing pancreatitis with reference to growth hormone treatment

Objective To observe the expression of C D44 mRNA and investigate its relation with T lymphocytes (CD3/CD4/CD8) and histo logical changes in the rat intestinal mucosa during acute necrotizing pancreatit is (ANP) and the influence of growth hormone (GH) treatment. Methods Fifty-four r ats were randomly divided into three groups: sham operation (SO) group, ANP group, ANP GH group (GH: 0.7 5 U/kg). ANP model was made by injection of 5 % sodium taurocholate into biliopa ncreatic duct in rats. These rats were sacrificed at 6, 12, 24 h and intestinal mucosa were harvested for the determination of CD44mRNA expression by using RT -PCR and CD3/CD4/CD8 cells counting by immunohistochemistry technique. Patholog ical changes of rat intestinal mucosa were also observed. Results The expression o f CD44 mRNA in intestinal mucosa of ANP group was decreased as compared with tha t in SO group (P<0.05). GH treatment markedly upregulated CD44 mRNA expressi on. CD3/CD4/CD8 cells in ANP group were also decreased almost at all time points when compared with SO group (P<0.05). There was no significant difference i n CD3/CD4/CD8 cells between GH-treatment group and SO group (P>0.05). The i ntestinal mucosa were severely damaged in ANP group but preserved well in GH-tr eatment group. Conclusion The expression of CD44mRNA in intestinal m ucosa was decreased during ANP. The mechanisms by which GH protected intestinal barrier might include strengthening cell immune function and cell-extracellular matrix binding by upregulating CD44mRNA expression.