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


CONCLUSIONS
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.
Department of Electronic Engineering, Chengdu University of Information Technology, Chengdu 610225, China.
Yong-hong
YH
Li
Fu-qian
FQ
He
Zong-wen
ZW
Huang
Ping
P
Xue
Qing
Q
Xia
D000818:Animals; D004642:Emodin / Q000494:pharmacology / Q000627:therapeutic use*; D005260:Female; D005772:Gastrointestinal Transit / Q000187:drug effects*; D053583:Interleukin-1beta / Q000378:metabolism; D007413:Intestinal Mucosa / Q000187:drug effects / Q000473:pathology; D007421:Intestine, Small / Q000378:metabolism / Q000473:pathology*; D008297:Male; D016328:NF-kappa B / Q000378:metabolism; D019283:Pancreatitis, Acute Necrotizing / Q000188:drug therapy* / Q000473:pathology*; D020011:Protective Agents / Q000494:pharmacology / Q000627:therapeutic use; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D053583:Interleukin-1beta; D016328:NF-kappa B; D020011:Protective Agents; D014409:Tumor Necrosis Factor-alpha; D004642:Emodin