大黄素对急性坏死性胰腺炎大鼠肠道损伤的保护作用

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目的研究大黄素对急性坏死性胰腺炎(ANP)大鼠肠道损伤的保护机制。方法将30只SD大鼠随机分成3组:假手术(SO)组、ANP组和大黄素治疗组,每组10只。ANP模型采用十二指肠壁穿刺经乳头逆行胰胆管注射3.5%牛磺胆酸钠造模,5.5h后从十二指肠注入酚红,0.5h后处死大鼠,测定小肠转运。取小肠组织做病理切片,HE染色观察小肠组织病理改变,免疫组织化学染色检测小肠核因子-κB(NF-κB)的活化;用酶标记免疫吸附测定法(ELISA)检测小肠肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)。结果 ANP组小肠转运较SO组降低(P<0.05),大黄素治疗组小肠转运较ANP组增加(P<0.05)。SO组肠黏膜无异常,ANP组大鼠肠黏膜水肿、出血及炎症细胞浸润,大黄素治疗组大鼠肠黏膜轻度水肿,黏膜及黏膜下层血管扩张充血及炎症细胞浸润相对ANP组减轻。ANP组小肠黏膜细胞胞核NF-κBp65阳性表达量高于SO组(P<0.05),大黄素治疗组较ANP组降低(P<0.05)。ANP组小肠TNF-α、IL-1β含量较SO组增加(P<0.05),大黄素治疗组较ANP组降低但高于SO组(P<0.05)。小肠TNF-α、IL-1β与小肠转运呈负相关,r分别为-0.83、-0.76(P<0.05)。结论大黄素可增加小肠转运,抑制ANP大鼠小肠NF-κB活性,降低小肠TNF-α、IL-1β含量,减轻小肠病理损害。 Objective To study the protective mechanism of emodin on intestinal injury in acute necrotizing pancreatitis (ANP) rats. Methods Thirty SD rats were randomly divided into three groups: sham operation (SO) group, ANP group and emodin treatment group, 10 in each group. ANP model using duodenal wall puncture retrograde injection of 3.5% sodium taurocholate through the nipple, 5.5 h after injection of phenol red from the duodenum, 0.5 h after the rats were killed to determine the intestinal transit. Small intestine tissue was taken for pathological section, HE staining was used to observe the pathological changes of the small intestine, immunohistochemical staining was used to detect the activation of nuclear factor-κB (NF-κB) in the small intestine, and small intestinal tumor necrosis factor-α was detected by enzyme-labeled immunosorbent assay (ELISA). (TNF-α) and interleukin-1β (IL-1β). Results Small intestine transport in ANP group was lower than that in SO group (P<0.05). Small intestine transport in emodin group was higher than that in ANP group (P<0.05). There was no intestinal mucosal abnormality in the SO group. Intestinal mucosal edema, hemorrhage, and inflammatory cell infiltration were observed in the ANP group. Mild edema of the intestinal mucosa was observed in the emodin-treated group. Dilation and congestion of blood vessels in the mucosa and submucosa and inflammatory cell infiltration were alleviated compared with the ANP group. The positive expression level of NF-κBp65 in the nucleus of intestinal mucosa in ANP group was higher than that in SO group (P<0.05). The emodin treatment group was lower than that in ANP group (P<0.05). The content of TNF-α and IL-1β in the small intestine of ANP group was higher than that of SO group (P<0.05). The emodin treatment group was lower than the ANP group but higher than the SO group (P<0.05). Intestinal transport of TNF-α and IL-1β was negatively correlated with small intestine transport, r was -0.83 and -0.76, respectively (P<0.05). Conclusion Emodin can increase the intestinal transit, inhibit the activity of NF-κB in the small intestine of ANP rats, reduce the content of TNF-α and IL-1β in the small intestine, and reduce the intestinal pathological damage.
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