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Journal of Zhejiang University SCIENCE B 2008 Vol.9 No.4 P.341-350

http://doi.org/10.1631/jzus.B0720198


Sodium arsenite reduces severity of dextran sulfate sodium-induced ulcerative colitis in rats


Author(s):  Joshua J. MALAGO, Hortensia NONDOLI

Affiliation(s):  Department of Pathology, Faculty of Veterinary Medicine, Sokoine University of Agriculture, P.O. Box 3203, Morogoro, Tanzania; more

Corresponding email(s):   malagojj@yahoo.com, jmalago@suanet.ac.tz

Key Words:  Ulcerative colitis, Dextran sulfate sodium, Sodium arsenite, Rats


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Joshua J. MALAGO, Hortensia NONDOLI. Sodium arsenite reduces severity of dextran sulfate sodium-induced ulcerative colitis in rats[J]. Journal of Zhejiang University Science B, 2008, 9(4): 341-350.

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journal="Journal of Zhejiang University Science B",
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doi="10.1631/jzus.B0720198"
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%T Sodium arsenite reduces severity of dextran sulfate sodium-induced ulcerative colitis in rats
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%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B0720198

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T1 - Sodium arsenite reduces severity of dextran sulfate sodium-induced ulcerative colitis in rats
A1 - Joshua J. MALAGO
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EP - 350
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PB - Zhejiang University Press & Springer
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DOI - 10.1631/jzus.B0720198


Abstract: 
The histopathological features and the associated clinical findings of ulcerative colitis (UC) are due to persistent inflammatory response in the colon mucosa. Interventions that suppress this response benefit UC patients. We tested whether sodium arsenite (SA) benefits rats with dextran sulfate sodium (DSS)-colitis. The DSS-colitis was induced by 5% DSS in drinking water. SA (10 mg/kg; intraperitoneally) was given 8 h before DSS treatment and then every 48 h for 3 cycles of 7, 14 or 21 d. At the end of each cycle rats were sacrificed and colon sections processed for histological examination. DSS induced diarrhea, loose stools, hemoccult positive stools, gross bleeding, loss of body weight, loss of epithelium, crypt damage, depletion of goblet cells and infiltration of inflammatory cells. The severity of these changes increased in the order of Cycles 1, 2 and 3. Treatment of rats with SA significantly reduced this severity and improved the weight gain.

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Reference

[1] Arai, Y., Takanashi, H., Kitagawa, H., Okayasu, I., 1998. Involvement of interleukin-1 in the development of ulcerative colitis induced by dextran sulfate sodium in mice. Cytokine, 10(11):890-896.

[2] Chen, D., Pan, J., Du, B., Sun, D., 2005. Induction of the heat shock response in vivo inhibits NF-kappa B activity and protects murine liver from endotoxemia-induced injury. J. Clin. Immunol., 25(5):452-461.

[3] Chen, Y., Si, J.M., Liu, W.L., Cai, J.T., Du, Q., Wang, L., Liang, J., Gao, M., 2007. Induction of experimental acute ulcerative colitis in rats by administration of dextran sulfate sodium at low concentration followed by intracolonic administration of 30% ethanol. J. Zhejiang Univ. Sci. B, 8(9):632-637.

[4] Cooper, H.S., Murthy, S.N., Shah, R.S., Sedergran, D.J., 1993. Clinicopathologic study of dextran sulfate sodium experimental murine colitis. Lab. Invest., 69(2):238-249.

[5] Gaudio, E., Taddei, G., Vetuschi, A., Sferra, R., Frieri, G., Ricciardi, G., Caprilli, R., 1999. Dextran sulfate sodium colitis in rats: clinical, structural and ultrastructural aspects. Dig. Dis. Sci., 44(7):1458-1475.

[6] Hata, K., Andoh, A., Sato, H., Araki, Y., Tanaka, M., Tsujikawa, T., Fujiyama, Y., Bamba, T., 2001. Sequential changes in luminal microflora and mucosal cytokine expression during developing of colitis in HLA-B27/beta2-microglobulin transgenic rats. Scand. J. Gastroenterol., 36(11):1185-1192.

[7] Hecht, G., Savkovic, S.D., 1997. Effector role of epithelia in inflammation: interaction with bacteria. Aliment. Pharmacol. Ther. (Suppl.), 3:64-69.

[8] Herias, M.V., Koninkx, J.F.J.G., Vos, J.G., Huis in't Veld, J.H.J., van Dijk, J.E., 2005. Probiotic effects of Lactobacillus casei on DSS-induced ulcerative colitis in mice. IJFM, 103(2):143-155.

[9] Iba, Y., Sugimoto, Y., Kamei, C., Masukawa, T., 2003. Possible role of mucosal mast cells in the recovery process of colitis induced by dextran sulfate sodium in rats. Int. Immunopharmacol., 3(4):485-491.

[10] Kullmann, F., Messmann, H., Alt, M., Gross, V., Bocker, T., Scholmerich, J., Ruschoff, J., 2001. Clinical and histopathological features of dextran sulfate sodium induced acute and chronic colitis associated with dysplasia in rats. Int. J. Colorectal Dis., 16(4):238-246.

[11] Lee, K.J., Hahn, G.M., 1988. Abnormal proteins as the trigger for the induction of stress responses: heat, diamide, and sodium arsenite. J. Cell. Physiol., 136(3):411-420.

[12] Lowenstein, D.H., Chan, P.H., Miles, M.F., 1991. The stress protein response in cultured neurons: characterization and evidence for a protective role in excitotoxicity. Neuron, 7(6):1053-1060.

[13] Malago, J.J., 2003. The Role of the Heat Shock Response in the Cytoprotection of the Intestinal Epithelium. Ph.D Thesis, Wijk bij Duurstede, Addix.

[14] Malago, J.J., Koninkx, J.F.J.G., van Dijk, J.E., 2002. The heat shock response and cytoprotection of intestinal epithelium. Cell Stress Chaperones, 7(2):191-199.

[15] Malago, J.J., Koninkx, J.F.J.G., Ovelgönne, H.H., van Asten, F.J.A.M., Swennenhuis, J.F., van Dijk, J.E., 2003. Expression levels of heat shock proteins in enterocyte-like Caco-2 cells after exposure to Salmonella enteritidis. Cell Stress Chaperones, 8(2):194-203.

[16] Marrero, J.A., Matkowskyj, K.A., Yung, K., Hecht, G., Benya, R.V., 2000. Dextran sulfate sodium-induced murine colitis activates NF-κB and increases galanin-1 receptor expression. Am. J. Physiol. Gastrointest. Liver Physiol., 278(5):G797-G804.

[17] Murthy, S.N.S., Cooper, H.S., Shim, H., Shah, R.S., Ibrahim, S.A., Sedergran, D.J., 1993. Treatment of dextran sulfate sodium-induced murine colitis by intracolonic cyclosporin. Dig. Dis. Sci., 38(9):1722-1734.

[18] Nover, L., 1991. HSFs and HSPs—a stressful program on transcription factors and chaperones. New Biol., 3(9):855-859.

[19] Okayasu, I., Hatakeyama, S., Yamada, M., Ohkusa, T., Inagaki, Y., Nakaya, R., 1990. A novel method in the induction of reliable experimental acute and chronic ulcerative colitis in mice. Gastroenterology, 98(3):694-702.

[20] Podolsky, D.K., 1991. Inflammatory bowel disease. N. Engl. J. Med., 325(13):928-937.

[21] Pritts, T.A., Wang, Q., Sun, X., Fischer, D.R., Hungness, E.S., Fischer, J.E., Wong, H.R., Hasselgren, P.O., 2002. The stress response decreases NF-kappa B activation in liver of endotoxemic mice. Shock, 18(1):33-37.

[22] Ribeiro, S.P., Villar, J., Downey, G.P., Edelson, J.D., Slutsky, A.S., 1994. Sodium arsenite induces heat shock protein 72 kilodalton expression in the lungs and protects rats against sepsis. Crit. Care Med., 22(6):922-929.

[23] Venkatraman, A., Ramakrishna, B.S., Pulimood, A.B., Patra, S., Murthy, S., 2000. Increased permeability in dextran sulphate colitis in rats: time course of development and effect of butyrate. Scand. J. Gastroenterol., 35(10):1053-1059.

[24] Vetuschi, A., Latella, G., Sferra, R., Caprilli, R., Gaudio, E., 2002. Increased proliferation and apoptosis of colonic epithelial cells in DSS-induced colitis in rats. Dig. Dis. Sci., 47(7):1447-1457.

[25] Wang, Q., Hasselgren, P.O., 2002. Heat shock response reduces intestinal permeability in septic mice: potential role of interleukin-10. Am. J. Physiol. Regul. Integr. Comp. Physiol., 282(3):R669-R676.

[26] Welch, W.J., 1992. Mammalian stress response: cell physiology, structure/function of stress proteins, and implications for medicine and disease. Physiol. Rev., 72(4):1063-1081.

[27] Wiegant, F.A., Souren, J.E., van Rijn, H., van Wijk, R., 1993. Arsenite induced sensitization and self-tolerance of Reuber H35 hepatoma cells. Cell Biol. Toxicol., 9(1):49-59.

[28] Wijeweera, J.B., Thomas, C.M., Gandolfi, A.J., Brendel, K., 1995. Sodium arsenite and heat shock induce stress proteins in precision-cut rat liver slices. Toxicology, 104(1-3):35-45.

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