大黄素对重症急性胰腺炎大鼠肠黏膜细胞凋亡和血清瘦素表达的影响

目的：探讨大黄素对重症急性胰腺炎大鼠肠黏膜屏障的保护机制。方法：60只成年SD大鼠随机分为假手术组、模型组和大黄素组。通过3％牛磺胆酸钠逆行胰胆管注射建立重症急性胰腺炎模型。造模成功后24h门静脉取血，检测血清瘦素含量、淀粉酶活性及血浆内毒素含量。取近回盲部回肠黏膜组织，光学显微镜、电子显微镜下观察肠黏膜病理学改变及超微结构改变；细胞凋亡原位标记法检测回肠黏膜上皮细胞凋亡率，免疫组织化学法检测回肠黏膜组织中Bax蛋白的表达情况。结果：术后模型组血浆内毒素含量、血清瘦素含量、血清淀粉酶活性、Bax蛋白表达及肠黏膜细胞凋亡率均显著高于假手术组（P〈0．01），而大黄素组血浆内毒素含量、血清淀粉酶活性、Bax蛋白表达和肠黏膜细胞凋亡率则明显低于模型组（P〈0．01），血清瘦素水平较模型组明显升高（P〈0．05）。模型组胰腺和肠黏膜的病理损害较假手术组加重，而大黄素组病理损害较模型组减轻。结论：大黄素通过抑制肠黏膜上皮细胞过度凋亡，上调血清瘦素水平，达到维持肠黏膜屏障完整性的功效，进而抑制重症急性胰腺炎细菌内毒素移位。

Effects of emodin on cell apoptosis of intestinal mucosa and serum leptin in rats with severe acute pancreatitis

Objective： To explore the mechanisms of emodin in protecting intestinal mucosal barrier in rat with severe acute pancreatitis （SAP）. Methods： Sixty SD rats were randomly divided into three groups： sham-operation group, untreated group, and emodin group. SAP in rats of the untreated group and the emodin group was induced by retrograde pumping of 3.0% sodium chelate to the common bile duct. Specimens were obtained 24 hours after the severe acute pancreatitis was induced. Serum level of leptin, serum activity of amylase and plasma content of endotoxin were measured. Ileum mucosa from ileocecal junction was observed by light microscopy and electron microscopy to measure pathological and ultrastructural changes. Apoptosis of ileum mucosal cells was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling method, and expression of Bax in ileum mucosal cells was measured by immunohistochemical method. Results： Compared with the sham-operation group, there was significant increase in the levels of leptin, endotoxin, the activity of amylase, apoptosis index and Bax expression in the untreated group （P〈0. 01）. Compared with the untreated group, the level of endotoxin, apoptotic index and Bax expression level in the emodin group were significantly reduced （P〈0.01） and the leptin level was increased （P〈0.05）. More severe pathological changes appeared in the untreated group than in the sham-operation group under the light and electron microscopes; meanwhile less severe damage was observed in the emodin group as compared with the untreated group. Conclusion： Emodin can inhibit the apoptosis of intestinal mucosa cells and up-regulate the serum leptin content to protect the intestinal barrier function and prevent the translocation of bacteria and endotoxin.