摘要
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 explore the protective effects and mechanism of Emodin on intestinal lesion in the rats with acute necrotizing pancreatitis （ANP）. Methods Thirty SD rats were randomly divided into 3 groups： sham-operated （SO） group, ANP group and Emodin-treated group. ANP was induced by retro-pumping 3. 5% sodium cholate to pancreatieobiliary duct. 5.5 hours after modeling, phenol red, which was employed to measure intestinal transit, was injected to duodenum. 0.5 hour later, rats were sacrificed to collect intestine for the results of intestinal transit and other tests of intestine. Furthermore, intestinal tissue （HE staining） was observed by light microscope, and the activity of nuclear factor-kappa B （NF-κB） in intestine was detected by immunohistochemical method. The content of intestinal tumor necrosis factor-α （TNF-α） and interleukin-1β （IL-1β） was detected with the method of enzyme-labeled immunosorbent assay （ELISA）. Results Compared with SO group, there was significantly decrease of intestinal transit in ANG group （P〈0. 05）. Furthermore, intestinal transit in Emodintreated group significantly increased when compared with ANP group （P〈0. 05）. NF-BB p65 positive rate of intestinal cell nuclei, content of intestinal TNF-α and IL-1β in ANP group were obviously higher than those in SO group （P〈0.05）. After the treatment of Emodin, NF-κB p65 positive rate of intestinal cell nuclei, content of TNF- a and IL-1β were decreased （P〈0. 05）. Moreover, there was a negative correlation between intestinal transit and content of TNF-α, IL-1β, with correlation coefficients - 0. 83, - 0. 76, respectively （P 〈 0. 05）. Conclusion Emodin could increase intestinal transit, suppress the activity of NF-κB in intestine, decrease the content of intestinal TNF-α and IL-1β, and attenuate the pathological damage of intestine.
出处
《四川大学学报（医学版）》
CAS
CSCD
北大核心
2010年第6期1012-1015,共4页
Journal of Sichuan University(Medical Sciences)
基金
成都信息工程学院科研基金(项目编号:KYTZ201021)资助
