Full Text:   <2501>

CLC number: R657.51

On-line Access: 

Received: 2003-05-27

Revision Accepted: 2003-08-05

Crosschecked: 0000-00-00

Cited: 7

Clicked: 4783

Citations:  Bibtex RefMan EndNote GB/T7714

-   Go to

Article info.
1. Reference List
Open peer comments

Journal of Zhejiang University SCIENCE A 2004 Vol.5 No.4 P.477-482


Suppressing progress of pancreatitis through selective inhibition of NF-κB activation by using NAC

Author(s):  ZHAO Zhi-cheng, ZHENG Shu-sen, CHENG Wen-liang, WANG Xuan, QI Ying

Affiliation(s):  Dept. of Hepatobiliary Surgery, First Affiliated Hospital, Medical College, Zhejiang University, Hangzhou 310003, China; more

Corresponding email(s):   zc.zhao@163.com

Key Words:  Pancreatitis, NF-&kappa, B, TNF-&alpha

Share this article to: More

ZHAO Zhi-cheng, ZHENG Shu-sen, CHENG Wen-liang, WANG Xuan, QI Ying. Suppressing progress of pancreatitis through selective inhibition of NF-κB activation by using NAC[J]. Journal of Zhejiang University Science A, 2004, 5(4): 477-482.

@article{title="Suppressing progress of pancreatitis through selective inhibition of NF-κB activation by using NAC",
author="ZHAO Zhi-cheng, ZHENG Shu-sen, CHENG Wen-liang, WANG Xuan, QI Ying",
journal="Journal of Zhejiang University Science A",
publisher="Zhejiang University Press & Springer",

%0 Journal Article
%T Suppressing progress of pancreatitis through selective inhibition of NF-κB activation by using NAC
%A ZHAO Zhi-cheng
%A ZHENG Shu-sen
%A CHENG Wen-liang
%A WANG Xuan
%A QI Ying
%J Journal of Zhejiang University SCIENCE A
%V 5
%N 4
%P 477-482
%@ 1869-1951
%D 2004
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.2004.0477

T1 - Suppressing progress of pancreatitis through selective inhibition of NF-κB activation by using NAC
A1 - ZHAO Zhi-cheng
A1 - ZHENG Shu-sen
A1 - CHENG Wen-liang
A1 - WANG Xuan
A1 - QI Ying
J0 - Journal of Zhejiang University Science A
VL - 5
IS - 4
SP - 477
EP - 482
%@ 1869-1951
Y1 - 2004
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.2004.0477

Objective: To explore the characteristics of b%5D=abstract&ck%5b%5D=keyword'>b>NF-&kappa;b activation in the progress of b%5D=abstract&ck%5b%5D=keyword'>b>pancreatitis, the relationship with expression of TNF-&alpha; in the inflammatory reaction, and prevent the exacerbation of b%5D=abstract&ck%5b%5D=keyword'>b>pancreatitis by using NAC. Method: Forty-eight rats were divided into three groups: therapy (group C), b%5D=abstract&ck%5b%5D=keyword'>b>pancreatitis (group b) and control (group A). NAC served as the inhibitor of b%5D=abstract&ck%5b%5D=keyword'>b>NF-&kappa;b activation. In the time intervals of 1.5, 3.0, 6.0, 12.0 hour, b%5D=abstract&ck%5b%5D=keyword'>b>NF-&kappa;b activation was detected with flow cytometry (FCM) and the expression of TNF-&alpha; mRNA and protein with in situ hybridization (ISH) and enzyme-linked immuno-sorbent assay (ELISA) respectively. Meanwhile, the level of lipase and amylase in the serum was assayed and the pathological change was evaluated. Result: b%5D=abstract&ck%5b%5D=keyword'>b>NF-&kappa;b activation in the b%5D=abstract&ck%5b%5D=keyword'>b>pancreatitis group was higher than that in the control group (P<0.01), peaked at 3 hours, and was depressed by the inhibitor of b%5D=abstract&ck%5b%5D=keyword'>b>NF-&kappa;b, NAC. The expression of TNF-&alpha; as well as the level of lipase and amylase in the serum also rose synchronously with activation of b%5D=abstract&ck%5b%5D=keyword'>b>NF-&kappa;b. In contrast to group A, it was significantly different (P<0.01) in group b. After using NAC in group C, all of these values were decreased and the inflammatory reaction in the pancreas abated evidently. The pathology changes of the pancreas were shown to be alleviated in group C. Conclusion: First, b%5D=abstract&ck%5b%5D=keyword'>b>NF-&kappa;b activity is intensively initiated in the course of b%5D=abstract&ck%5b%5D=keyword'>b>pancreatitis and shown to have closely relationship with the release of cytokines. Second, use of NAC markedly depressed b%5D=abstract&ck%5b%5D=keyword'>b>NF-&kappa;b activation. TNF-&alpha; expression is down regulated by cytokines. It is suggested that NAC probably acts as a useful agent for treatment of b%5D=abstract&ck%5b%5D=keyword'>b>pancreatitis by indirectly inhibiting activation of b%5D=abstract&ck%5b%5D=keyword'>b>NF-&kappa;b.

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article


[1] Aho, H.J., Koskensalo, M.L., Nevalainen, T.J., 1980. Experimental pancreatitis in the rat: sodium taurocholate-induced acute haemorrhagic pancreatitis.Scand J Gastroenterol,15:411-416.

[2] Bhatnagar, A., Wig, J.D., Majumdar, S., 2001. Expression of activation, adhesion molecules and intracellular cytokines in acute pancreatitis.Immunology Letters, (77):133-141.

[3] Ethridge, R.T, Hashimoto, K., Chung, D.H., Ehlers, R.A., Rajaraman, S., Evers, B.M., 2002. Selective Inhibition of NF-κB Attenuates the Severity of Cerulein-Induced Acute Pancreatitis.J Am Coll Surg,195(4):497-505.

[4] Gross, V., Leser, H.G., Heinisch, A., Scholmeridu, J., 1993. Inflammatory mediators and cytokinesnew aspects of the pathophysiology and assessment of severity of acute pancreatitisHepato-Gastroenterology,40:522-530.

[5] Grewal, H.P., Kotb, M., el.Din, A.M., Ohman, M., Salem, A., Gaber, L., Gaber, A.O., 1994. Induction of tumor necrosis factor in severe acute pancreatitis and its subsqent reduction after hepatic passage.Surgery,115(2):213.

[6] Gukovsky, I., Gukovskaya, A.S., Blinman, T.A., Zaninovic, V., Pandol, S.J., 1998. Early NF kappa B activation is associated with hormone-induced pancreatitis.Am J Physiol,275:G1402-G1414.

[7] Kikucki, Y., Shimosigawa, T., Satoh, A., Abe, R., Abe, T., Koizumi, M., Toyota, T., 1996. The role of nitric oxide in mouse cerulein-induced pancreatitis with and without lipopolysaccharide pretreatment.Pancreas,12(1):68-75.

[8] Kim, H., Seo, J.Y., Roh, K.H., Lim, J.W., Kim, K.H., 2000. Suppression of NF-κB activation and cytokine production by N-acetylcysteine in pancreatic acinar cells.Free Radical Biology & Medicine,29(7):674-683.

[9] Lowry, S.F., 1993. Cytokine mediators of immunity and inflammation.Arch Surg,128:1235-1241.

[10] Norman, J., 1998. The role of cytokines in the pathogenesis of acute pancreatitis.Am. J.Surg,175:76-83.

[11] Norman, J., Fink, G., Denahm, W., 1997. Tissue specific cytokine production during experimental acute pancreatitis: a probable mechanism for distant organ dysfunction.Dig. Dis. Sci,42(8):1783-1788.

[12] Oliver, C., Waters, J. F., Tolbert, C. L., 1987. Growth of exocrine acinar cells on a reconstituted basement membrane gel.In Vitro Cell Dev. Biol,23:465-473.

[13] Pahl, H.L., 1999. Activation and target genes of Rel/NF-κB transcription factors.Oncogene,18:8653-8666.

[14] Pinkus, R., Weiner, L.M., Daniel, V., 1996. Role of oxidants and antioxidants in the induction of AP-1, NF-κB and glutathione S-transferase gene expression.J Biol Chem,271:13422-13429.

[15] Rongione, A.J., Kusske, A.M. Reber, H., Ashley, S.W., McFadden, D.W., 1997. Interleukin-10 reduces circulating levels of serum cytokines in experimental pancreatitis.J Gastrointel Surg,1(2):159-166.

[16] Schmidt, J., Lewandrowski, K., Fernandez-del Castillo, C., Mandavilli, U., Compton, C.C., Warshaw, A.L., Rattner, D.W., 1992. Histo-pathologic correlates of serum amylase activity in acute experimental pancreatitis.Dig Dis Sci,37(9):1426-1433.

[17] Steinle, A.U., Weidenbach, H., Wagner, M., Adler, G., Schmid, R.M., 1999. NF-κB/Rel activation in cerulein pancreatitis.Gastroenterology,116:420-430.

Open peer comments: Debate/Discuss/Question/Opinion


Please provide your name, email address and a comment

Journal of Zhejiang University-SCIENCE, 38 Zheda Road, Hangzhou 310027, China
Tel: +86-571-87952783; E-mail: cjzhang@zju.edu.cn
Copyright © 2000 - 2024 Journal of Zhejiang University-SCIENCE