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大黄素对急性坏死性胰腺炎大鼠模型肠道损伤的保护作用

[Protective effects of emodin on intestinal lesion in rat model with acute necrotizing pancreatitis].

作者信息

Li Yong-hong, He Fu-qian, Huang Zong-wen, Xue Ping, Xia Qing

机构信息

Department of Electronic Engineering, Chengdu University of Information Technology, Chengdu 610225, China.

出版信息

Sichuan Da Xue Xue Bao Yi Xue Ban. 2010 Nov;41(6):1012-5.

Abstract

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 pancreaticobiliary 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-kappaB) in intestine was detected by immunohistochemical method. The content of intestinal tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) 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 Emodin-treated group significantly increased when compared with ANP group (P < 0.05). NF-kappaB p65 positive rate of intestinal cell nuclei, content of intestinal TNF-alpha and IL-1beta in ANP group were obviously higher than those in SO group (P < 0.05). After the treatment of Emodin, NF-kappaB p65 positive rate of intestinal cell nuclei, content of TNF-alpha and IL-1beta were decreased (P < 0.05). Moreover, there was a negative correlation between intestinal transit and content of TNF-alpha, IL-1beta, with correlation coefficients--0.83, -0.76, respectively (P < 0.05).

CONCLUSION

Emodin could increase intestinal transit, suppress the activity of NF-kappaB in intestine, decrease the content of intestinal TNF-alpha and IL-1beta, and attenuate the pathological damage of intestine.

摘要

目的

探讨大黄素对急性坏死性胰腺炎(ANP)大鼠肠道损伤的保护作用及机制。

方法

将30只SD大鼠随机分为3组:假手术(SO)组、ANP组和大黄素治疗组。通过向胰胆管逆行注射3.5%胆酸钠诱导ANP。造模5.5小时后,将用于测量肠道传输的酚红注入十二指肠。0.5小时后,处死大鼠,收集肠道以进行肠道传输结果及其他肠道检测。此外,用光镜观察肠道组织(HE染色),并用免疫组化法检测肠道中核因子-κB(NF-κB)的活性。采用酶联免疫吸附测定(ELISA)法检测肠道肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)的含量。

结果

与SO组相比,ANP组肠道传输明显降低(P<0.05)。此外,与ANP组相比,大黄素治疗组肠道传输显著增加(P<0.05)。ANP组肠道细胞核NF-κB p65阳性率、肠道TNF-α和IL-1β含量明显高于SO组(P<0.05)。大黄素治疗后,肠道细胞核NF-κB p65阳性率、TNF-α和IL-1β含量降低(P<0.05)。此外,肠道传输与TNF-α、IL-1β含量呈负相关,相关系数分别为-0.83、-0.76(P<0.05)。

结论

大黄素可增加肠道传输,抑制肠道NF-κB活性,降低肠道TNF-α和IL-1β含量,减轻肠道病理损伤。

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