Ning Jian-wen, Ji Feng, Luo Dan-dong, Yang Chun-yan, Wang Li-jun
Department of Emergency, the First Affiliated Hospital of College of Medicine, Zhejiang University, Hangzhou 310003, Zhejiang Province, China.
Zhong Xi Yi Jie He Xue Bao. 2009 Dec;7(12):1167-73. doi: 10.3736/jcim20091215.
To explore the mechanisms of emodin in protecting intestinal mucosal barrier in rat with severe acute pancreatitis (SAP).
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 cholate 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.
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.
Emodin can inhibit the apoptosis of intestinal mucosa cells and up-regulate the serum leptin content to protect the intestina1 barrier function and prevent the translocation of bacteria and endotoxin.
探讨大黄素对重症急性胰腺炎(SAP)大鼠肠黏膜屏障的保护机制。
将60只SD大鼠随机分为三组:假手术组、未治疗组和大黄素组。未治疗组和大黄素组大鼠通过向胆总管逆行注入3.0%胆酸钠诱导SAP。在诱导重症急性胰腺炎24小时后获取标本。检测血清瘦素水平、血清淀粉酶活性和血浆内毒素含量。通过光学显微镜和电子显微镜观察回盲部的回肠黏膜,以测量病理和超微结构变化。采用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法检测回肠黏膜细胞凋亡,采用免疫组织化学方法检测回肠黏膜细胞中Bax的表达。
与假手术组相比,未治疗组的瘦素、内毒素水平、淀粉酶活性、凋亡指数和Bax表达均显著升高(P<0.01)。与未治疗组相比,大黄素组的内毒素水平、凋亡指数和Bax表达水平显著降低(P<0.01),瘦素水平升高(P<0.05)。在光学显微镜和电子显微镜下,未治疗组的病理变化比假手术组更严重;同时,与未治疗组相比,大黄素组的损伤较轻。
大黄素可抑制肠黏膜细胞凋亡,上调血清瘦素含量,保护肠道屏障功能,防止细菌和内毒素移位。