Is Curcumine Effect Comparable to 5- Aminosalicylic Acid or Budesonide on a Rat Model of Ulcerative Colitis Induced by Trinitrobenzene Sulfonic Acid?
Inflammatory bowel disease (IBD) is a chronic
relapsing-remitting condition that afflicts millions of people
throughout the world and impairs their daily functions and quality of
life. Treatment of IBD depends largely on 5-aminosalicylic acid (5-
ASA) and corticosteroids. The present study aimed to clarify the
effects of 5-aminosalicylic acid, budesonide and currcumin on 90
male albino rats against trinitrobenzene sulfonic acid (TNB) induced
colitis. TNB was injected intrarectally to 50 rats. The other 40 rats
served as control groups. Both 5-ASA (in a dose of 120 mg/kg) and
budesonide (in a dose of 0.1 mg/kg) were administered daily for one
week whereas currcumin was injected intraperitonially (in a dose of
30 mg/kg daily) for 14 days after injection of either TNB in the
colitis rats (group B) or saline in control groups (group A). The study
included estimation of macroscopic score index, histological
examination of H&E stained sections of the colonic tissue,
biochemical estimation of myeloperoxidase (MPO), nitric oxide
(NO), and caspase-3 levels, in addition to studying the effect of tested
drugs on colonic motility. It was found that budesonide and curcumin
improved mucosal healing, reduced both NO production and caspase-
3 level. They had the best impact on the disturbed colonic motility in
TNBS-model of colitis.
<p>[1] Goldman L, Ausiello D. Gastrointestinal diseases. In: Cecil Medicine.
23rd ed. Elsevier publication, 2008:951-1083.
[2] Hugot J, Zouali H, Lesage S, Thomas G. Etiology of inflammatory
bowel diseases. Int J Colorectal Dis. 1999; 14:2-9.
[3] Torres MI, Ríos A. Current view of the immunopathogenesis in
inflammatory bowel disease and its implications for therapy. World J
Gastroenterol 2008; 14(13):1972-80.
[4] Sartor RB. Mechanisms of disease: pathogenesis of Crohn's disease and
ulcerative colitis. Nature Clinical Practice Gastroenterology &
Hepatology 2006; 3:390-407.
[5] Schepper HU, De man JG, Moreels TG, Pelckmans PA, De Winter BY.
Gastrointestinal sensory and motor disturbances in inflammatory bowel
disease – clinical relevance and pathophysiological mechanisms.
Alimentary pharmacology and therapeutics 2008; 27(8):621-37.
[6] Boughton-Smith NK. Pathological and therapeutic implications for nitric
oxide in inflammatory bowel disease. Journal of the Royal Society of
Medicine 1994; 87:312–4.
[7] D'Argenio G, Farrace MG, Cosenza V, De Ritis F, Vall ND, Manguso F,
Piacentini M. Expression of apoptosis-related proteins in rat with
induced colitis. International Journal of Colorectal Disease 2004;
19(5):451-60.
[8] Mesmer UK, Reed JC, Brune B. Bcl-2 protects macrophages from nitric
oxide-induced apoptosis. J Biol Chem 1996; 271:20192–7.
[9] Iimura M, Nakamura T, Shinozaki S, Iizuka B, Inoue Y, Suzuki S,
Hayashi N. Bax is downregulated in inflamed colonic mucosa of
ulcerative colitis. Gut 2000; 47:228–35.
[10] Kern F, Almy T, Abbot F, Bogdonoff M. The motility of the distal colon
in nonspecific ulcerative colitis. Gastroenterology. 1951; 19:492-503.
[11] Vrees M, Pricolo V, Potenti F, Cao W. Abnormal motility in patients
with ulcerative colitis. The Role of Inflammatory Cytokines. Archives of
Surgury 2002; 137:439-46.
[12] Jacobson K, McHugh K, Collins SM. Experimental colitis alters
myenteric nerve function at inflamed and noninflamed sites in the rat.
Gastroenterology 1995; 109: 718-22.
[13] Martinsson T, Ljung T, Rubio C, Hellström P. Beneficial Effects of
Ropivacaine in Rat Experimental Colitis. Journal of Pharmacology and
Experimental Therapeutics 1999; 291(2):642-7.
[14] Zhang M, Deng C, Zheng J, Xia J, Sheng D. Curcumin inhibits
trinitrobenzene sulphonic acid-induced colitis in rats by activation of
peroxisome proliferator-activated receptor gamma. Int Immunophrmacol
2006; 6(8):1233-42.
[15] Morris GP, Beck PL, Herridge MS, Depew WT, Szewczuk MR, Wallace
JL. Hapten-induced model of chronic inflammation and ulceration in the
rat colon. Gastroenterology 1989 Mar; 96(3):795-803.
[16] Akcan A, Muhtaroglu S, Akgun H, Akyildiz H, Kucuk C, Sozuer E,
Yurci A, Yilmaz N. Ameliorative effects of bombesin and neurotensin
on trinitrobenzene sulphonic acid-induced colitis, oxidative damage and
apoptosis in rats. World J Gastroenterol. 2008; 14(8): 1222–30.
[17] Rachmielwitz D, Simon PL, Schwartz LW, Griswold DE, Fondacaro JD,
Wasserman MA. Inflammatory mediaors of experimental colitis in rats.
Gastroenterology 1989; 97: 326-37.
[18] Fiocchi C. Inflammatory bowel disease: etiology and pathogenesis.
Gastroenterology 1998; 115:182–205.
[19] Pravda J. Radical induction theory of ulcerative colitis. World J
Gastroenterol 2005; 11(16):2371-84.
[20] Li M, Johnson CP, Adams MB, Sarna SK. Ileal and colonic motor
activity in dextran sodium sulfate-induced colitis in conscious rats.
Gastroenterology 1999; 116: G4470-2.
[21] Shi XZ, Sarna SK. Inflammatory modulation of muscarinic receptor
activation in canine ileal circular muscle cells. Gastroenterology 1999;
112: 864-74.
[22] Grossi L, McHugh K, Collins SM. On the specificity of altered muscle
function in experimental colitis in rats. Gastroenterology 1993;
104:1049-56.
[23] Cao W, Fiocchi C, Pricolo V. Production of IL-1, hydrogen peroxide,
and nitric oxide by colonic mucosa decreases sigmoid smooth muscle
contractility in ulcerative colitis. Am J Physiol Cell Physiol 2005; 289:
C1408-16.
[24] Khan WI, Collins SM. Gut motor function: immunological control in
enteric infection and inflammation. Clin Exp Immunol. 2006; 143(3):
389–97.
[25] Venkataranganna MV, Rafiq M, Gopumadhavan S, Peer G, Babu UV,
Mitra SK. NCB-02 protects dinitrochlorobenzene-induced colitis
through down-regulation of NFκ‑B and iNOS. World J Gastroenterol
2007; 13(7):1103-7.
[26] Wallace JL, MacNaughton WK, Morris GP, Beck PL. Inhibition of
leukotriene synthesis markedly accelerates healing in rat model of
inflammatory bowel disease. Gastroenterology 1989; 98: 29-36.
[27] Egan LJ, Mays DC, Huntoon CJ, Bell MP, Pike MG, Sandborn WJ,
Lipsky J, McKean DJ. Inhibition of interleukin-1-stimulated NF-kappaB
RelA/p65 phosphorylation by mesalamine is accompanied by decreased
transcriptional activity. J Biol Chem. 1999; 274:26448–53.
[28] Dubuquoy L, Dharancy S, Nutten S, Pettersson S, Auwerx J,
Desreumaux P. Role of peroxisome proliferator-activated receptor
gamma and retinoid X receptor heterodimer in hepatogastroenterological
diseases. Lancet 2002; 360:1410–8.
[29] Delerive P, De Bosscher K, Besnard S, Vanden Berghe W, Peters JM,
Gonzalez FJ, Fruchart JC, Tedgui A, Haegeman G, Staels B. Peroxisome
proliferator-activated receptor negatively regulates the vascular
inflammatory gene response by negative cross-talk with transcription
factors NF-B and AP-1. J Biol Chem 1999; 274: 32048–54.
[30] Sandoval M, Liu X, Mannick E, Clark D, Miller MJ. Peroxynitriteinduced
apoptosis in human intestinal epithelial cells is attenuated by
mesalamine. Gastroenterology 1997; 113(5):1480-8.
[31] Dubuquoy L, Rosseaux C, Thueru X. PPARγ as a new therapeutic target
in inflammatory bowel diseases, Gut 2006, 55:1341–9.
[32] Rust C, Bauchmuller K, Bernt C, Vennegeerts T, Fickert P, Fuchsbichler
A, Beuers U. Sulfasalazine reduces bile acid induced apoptosis in human
hepatoma cells and perfused rat livers. Gut 2006; 55:719-27.
[33] Barnes PJ, Karin M. Nuclear factor-kappa B: a pivotal transcription
factor in chronic inflammatory diseases. N Engl J Med 1997; 336: 1066–
71.
[34] De Bosscher, K., Haegeman, G. Minireview: Latest perspectives on
antiinflammatory actions of glucocorticoids. Mol. Endocrinol 2009; 23:
281-91.
[35] Moghadam A, Simoncini T, Yang Z, Limbourg F, Plumier J, Rebsamen
M. Acute cardiovascular protective effects of corticosteroids are
mediated by non-transcriptional activation of endothelial nitric oxide
synthase. Nat Med. 2002; 8(5): 473–9.
[36] Yu Z, Ouyang JP, Li YP. Dexamethasone attenuated endotoxin-induced
acute lung injury through inhibiting expression of inducible nitric oxide
synthase. Hem. Microcirc. 2009; 41(2):117-25.
[37] Wen LP, Madani K, Fahrni JA, Duncan SR, Rosen GD. Dexamethasone
inhibits lung epithelial cell apoptosis induced by IFN-γ and Fas. Am J
Physiol 1997; 273: L921-9.
[38] Yamamoto M, Fukuda K, Miura N, Suzuki R, Kido T, Komatsu Y.
Inhibition by dexamethasone of transforming growth factor ß1-induced
apoptosis in rat hepatoma cells: a possible association with bcl-xL
induction. Hepatology 1998; 27:959–66.
[39] Wang Z, Kang JS, Li Y, Yuan ZX, Liu SS, Sun LK. The effects of
dexamethasone on rat brain cortical nuclear factor kappa B in endotoxic
shock. Toxicol Appl Pharmacol. 2006; 214(3):263-9.
[40] Ammon H, Wahl M. Pharmacology of Curcuma longa. Planta Med.
1991; 57:1–6.
[41] Arbiser J, Klauber N, Rohan R, Van Leeuwen R, Huang M, Fischer C,
Flynn E, Byers H. Curcumin is an in vivo inhibitor of angigenesis. Mol.
Med. 1998; 4:376–383.
[42] Sugimoto k, H. Hanai, K. Tozawa, T. Aoshi, M. Uchijima, T. Nagata et
al., Curcumin prevents and ameliorates trinitrobenzene sulfonic acidinduced
colitis in mice, Gastroenterology 2002; 123:1912–22.
[43] Surh Y-J, Chun K-S, Cha H-H. Molecular mechanisms underlying
chemo-preventive activities of anti-inflammatory phytochemicals:
downregulation of COX-2 and iNOS through suppression of NF-B
activation. Mutat Res. 2001; 54:243-268.
[44] Dunsmore KE, Chen PG, Wong HR. Curcumin, a medicinal herbal
compound capable of inducing the heat shock response. Crit Care Med.
2001; 29:2199 204.
[45] Wallace JM. Nutritional and botanical modulation of the inflammatory
cascade—eicosanoids, cyclooxygenases and lipooxygenases—as an
adjunct in cancer therapy. Integr Cancer Ther. 2002; 1:7-37.
[46] Jian Y, Mai G, Wang J, Zhang Y, Luo R, Fang Y. Preventive and
therapeutic effects of NF-kappaB inhibitor curcumin in rats colitis
induced by trinitrobenzene sulfonic acid, World J Gastroenterol 2005;
11:1747–52.
[47] Jobin C, Bradham CA, Russo MP, Juma B, Narula AS, Brenner DA,
Sartor RB. Curcumin blocks cytokine-mediated NF-κB activation and
proinflammatory gene expression by inhibiting inhibitory factor I-κB
kinase activity. J Immunol. 1999; 163:3474–83.
[48] Karin M. Nuclear factor-κB in cancer development and progression.
Nature. 2006; 441:431–6.
[49] Menon V, Sudheer A. In: advances in experimental medicine and
biology-The Molecular Targets and Therapeutic Uses of Curcumin in
Health and Disease. Springer US 2007:105-25.
[50] Collins SM, Assche GV, Hogaboam C. Alterations in enteric nerve and
smooth-muscle function in inflammatory bowel diseases. Inflammatory
Bowel Diseases 1997; 3(1):38-48.</p>
<p>[1] Goldman L, Ausiello D. Gastrointestinal diseases. In: Cecil Medicine.
23rd ed. Elsevier publication, 2008:951-1083.
[2] Hugot J, Zouali H, Lesage S, Thomas G. Etiology of inflammatory
bowel diseases. Int J Colorectal Dis. 1999; 14:2-9.
[3] Torres MI, Ríos A. Current view of the immunopathogenesis in
inflammatory bowel disease and its implications for therapy. World J
Gastroenterol 2008; 14(13):1972-80.
[4] Sartor RB. Mechanisms of disease: pathogenesis of Crohn's disease and
ulcerative colitis. Nature Clinical Practice Gastroenterology &
Hepatology 2006; 3:390-407.
[5] Schepper HU, De man JG, Moreels TG, Pelckmans PA, De Winter BY.
Gastrointestinal sensory and motor disturbances in inflammatory bowel
disease – clinical relevance and pathophysiological mechanisms.
Alimentary pharmacology and therapeutics 2008; 27(8):621-37.
[6] Boughton-Smith NK. Pathological and therapeutic implications for nitric
oxide in inflammatory bowel disease. Journal of the Royal Society of
Medicine 1994; 87:312–4.
[7] D'Argenio G, Farrace MG, Cosenza V, De Ritis F, Vall ND, Manguso F,
Piacentini M. Expression of apoptosis-related proteins in rat with
induced colitis. International Journal of Colorectal Disease 2004;
19(5):451-60.
[8] Mesmer UK, Reed JC, Brune B. Bcl-2 protects macrophages from nitric
oxide-induced apoptosis. J Biol Chem 1996; 271:20192–7.
[9] Iimura M, Nakamura T, Shinozaki S, Iizuka B, Inoue Y, Suzuki S,
Hayashi N. Bax is downregulated in inflamed colonic mucosa of
ulcerative colitis. Gut 2000; 47:228–35.
[10] Kern F, Almy T, Abbot F, Bogdonoff M. The motility of the distal colon
in nonspecific ulcerative colitis. Gastroenterology. 1951; 19:492-503.
[11] Vrees M, Pricolo V, Potenti F, Cao W. Abnormal motility in patients
with ulcerative colitis. The Role of Inflammatory Cytokines. Archives of
Surgury 2002; 137:439-46.
[12] Jacobson K, McHugh K, Collins SM. Experimental colitis alters
myenteric nerve function at inflamed and noninflamed sites in the rat.
Gastroenterology 1995; 109: 718-22.
[13] Martinsson T, Ljung T, Rubio C, Hellström P. Beneficial Effects of
Ropivacaine in Rat Experimental Colitis. Journal of Pharmacology and
Experimental Therapeutics 1999; 291(2):642-7.
[14] Zhang M, Deng C, Zheng J, Xia J, Sheng D. Curcumin inhibits
trinitrobenzene sulphonic acid-induced colitis in rats by activation of
peroxisome proliferator-activated receptor gamma. Int Immunophrmacol
2006; 6(8):1233-42.
[15] Morris GP, Beck PL, Herridge MS, Depew WT, Szewczuk MR, Wallace
JL. Hapten-induced model of chronic inflammation and ulceration in the
rat colon. Gastroenterology 1989 Mar; 96(3):795-803.
[16] Akcan A, Muhtaroglu S, Akgun H, Akyildiz H, Kucuk C, Sozuer E,
Yurci A, Yilmaz N. Ameliorative effects of bombesin and neurotensin
on trinitrobenzene sulphonic acid-induced colitis, oxidative damage and
apoptosis in rats. World J Gastroenterol. 2008; 14(8): 1222–30.
[17] Rachmielwitz D, Simon PL, Schwartz LW, Griswold DE, Fondacaro JD,
Wasserman MA. Inflammatory mediaors of experimental colitis in rats.
Gastroenterology 1989; 97: 326-37.
[18] Fiocchi C. Inflammatory bowel disease: etiology and pathogenesis.
Gastroenterology 1998; 115:182–205.
[19] Pravda J. Radical induction theory of ulcerative colitis. World J
Gastroenterol 2005; 11(16):2371-84.
[20] Li M, Johnson CP, Adams MB, Sarna SK. Ileal and colonic motor
activity in dextran sodium sulfate-induced colitis in conscious rats.
Gastroenterology 1999; 116: G4470-2.
[21] Shi XZ, Sarna SK. Inflammatory modulation of muscarinic receptor
activation in canine ileal circular muscle cells. Gastroenterology 1999;
112: 864-74.
[22] Grossi L, McHugh K, Collins SM. On the specificity of altered muscle
function in experimental colitis in rats. Gastroenterology 1993;
104:1049-56.
[23] Cao W, Fiocchi C, Pricolo V. Production of IL-1, hydrogen peroxide,
and nitric oxide by colonic mucosa decreases sigmoid smooth muscle
contractility in ulcerative colitis. Am J Physiol Cell Physiol 2005; 289:
C1408-16.
[24] Khan WI, Collins SM. Gut motor function: immunological control in
enteric infection and inflammation. Clin Exp Immunol. 2006; 143(3):
389–97.
[25] Venkataranganna MV, Rafiq M, Gopumadhavan S, Peer G, Babu UV,
Mitra SK. NCB-02 protects dinitrochlorobenzene-induced colitis
through down-regulation of NFκ‑B and iNOS. World J Gastroenterol
2007; 13(7):1103-7.
[26] Wallace JL, MacNaughton WK, Morris GP, Beck PL. Inhibition of
leukotriene synthesis markedly accelerates healing in rat model of
inflammatory bowel disease. Gastroenterology 1989; 98: 29-36.
[27] Egan LJ, Mays DC, Huntoon CJ, Bell MP, Pike MG, Sandborn WJ,
Lipsky J, McKean DJ. Inhibition of interleukin-1-stimulated NF-kappaB
RelA/p65 phosphorylation by mesalamine is accompanied by decreased
transcriptional activity. J Biol Chem. 1999; 274:26448–53.
[28] Dubuquoy L, Dharancy S, Nutten S, Pettersson S, Auwerx J,
Desreumaux P. Role of peroxisome proliferator-activated receptor
gamma and retinoid X receptor heterodimer in hepatogastroenterological
diseases. Lancet 2002; 360:1410–8.
[29] Delerive P, De Bosscher K, Besnard S, Vanden Berghe W, Peters JM,
Gonzalez FJ, Fruchart JC, Tedgui A, Haegeman G, Staels B. Peroxisome
proliferator-activated receptor negatively regulates the vascular
inflammatory gene response by negative cross-talk with transcription
factors NF-B and AP-1. J Biol Chem 1999; 274: 32048–54.
[30] Sandoval M, Liu X, Mannick E, Clark D, Miller MJ. Peroxynitriteinduced
apoptosis in human intestinal epithelial cells is attenuated by
mesalamine. Gastroenterology 1997; 113(5):1480-8.
[31] Dubuquoy L, Rosseaux C, Thueru X. PPARγ as a new therapeutic target
in inflammatory bowel diseases, Gut 2006, 55:1341–9.
[32] Rust C, Bauchmuller K, Bernt C, Vennegeerts T, Fickert P, Fuchsbichler
A, Beuers U. Sulfasalazine reduces bile acid induced apoptosis in human
hepatoma cells and perfused rat livers. Gut 2006; 55:719-27.
[33] Barnes PJ, Karin M. Nuclear factor-kappa B: a pivotal transcription
factor in chronic inflammatory diseases. N Engl J Med 1997; 336: 1066–
71.
[34] De Bosscher, K., Haegeman, G. Minireview: Latest perspectives on
antiinflammatory actions of glucocorticoids. Mol. Endocrinol 2009; 23:
281-91.
[35] Moghadam A, Simoncini T, Yang Z, Limbourg F, Plumier J, Rebsamen
M. Acute cardiovascular protective effects of corticosteroids are
mediated by non-transcriptional activation of endothelial nitric oxide
synthase. Nat Med. 2002; 8(5): 473–9.
[36] Yu Z, Ouyang JP, Li YP. Dexamethasone attenuated endotoxin-induced
acute lung injury through inhibiting expression of inducible nitric oxide
synthase. Hem. Microcirc. 2009; 41(2):117-25.
[37] Wen LP, Madani K, Fahrni JA, Duncan SR, Rosen GD. Dexamethasone
inhibits lung epithelial cell apoptosis induced by IFN-γ and Fas. Am J
Physiol 1997; 273: L921-9.
[38] Yamamoto M, Fukuda K, Miura N, Suzuki R, Kido T, Komatsu Y.
Inhibition by dexamethasone of transforming growth factor ß1-induced
apoptosis in rat hepatoma cells: a possible association with bcl-xL
induction. Hepatology 1998; 27:959–66.
[39] Wang Z, Kang JS, Li Y, Yuan ZX, Liu SS, Sun LK. The effects of
dexamethasone on rat brain cortical nuclear factor kappa B in endotoxic
shock. Toxicol Appl Pharmacol. 2006; 214(3):263-9.
[40] Ammon H, Wahl M. Pharmacology of Curcuma longa. Planta Med.
1991; 57:1–6.
[41] Arbiser J, Klauber N, Rohan R, Van Leeuwen R, Huang M, Fischer C,
Flynn E, Byers H. Curcumin is an in vivo inhibitor of angigenesis. Mol.
Med. 1998; 4:376–383.
[42] Sugimoto k, H. Hanai, K. Tozawa, T. Aoshi, M. Uchijima, T. Nagata et
al., Curcumin prevents and ameliorates trinitrobenzene sulfonic acidinduced
colitis in mice, Gastroenterology 2002; 123:1912–22.
[43] Surh Y-J, Chun K-S, Cha H-H. Molecular mechanisms underlying
chemo-preventive activities of anti-inflammatory phytochemicals:
downregulation of COX-2 and iNOS through suppression of NF-B
activation. Mutat Res. 2001; 54:243-268.
[44] Dunsmore KE, Chen PG, Wong HR. Curcumin, a medicinal herbal
compound capable of inducing the heat shock response. Crit Care Med.
2001; 29:2199 204.
[45] Wallace JM. Nutritional and botanical modulation of the inflammatory
cascade—eicosanoids, cyclooxygenases and lipooxygenases—as an
adjunct in cancer therapy. Integr Cancer Ther. 2002; 1:7-37.
[46] Jian Y, Mai G, Wang J, Zhang Y, Luo R, Fang Y. Preventive and
therapeutic effects of NF-kappaB inhibitor curcumin in rats colitis
induced by trinitrobenzene sulfonic acid, World J Gastroenterol 2005;
11:1747–52.
[47] Jobin C, Bradham CA, Russo MP, Juma B, Narula AS, Brenner DA,
Sartor RB. Curcumin blocks cytokine-mediated NF-κB activation and
proinflammatory gene expression by inhibiting inhibitory factor I-κB
kinase activity. J Immunol. 1999; 163:3474–83.
[48] Karin M. Nuclear factor-κB in cancer development and progression.
Nature. 2006; 441:431–6.
[49] Menon V, Sudheer A. In: advances in experimental medicine and
biology-The Molecular Targets and Therapeutic Uses of Curcumin in
Health and Disease. Springer US 2007:105-25.
[50] Collins SM, Assche GV, Hogaboam C. Alterations in enteric nerve and
smooth-muscle function in inflammatory bowel diseases. Inflammatory
Bowel Diseases 1997; 3(1):38-48.</p>
@article{"International Journal of Medical, Medicine and Health Sciences:63533", author = "Inas E. Darwish and Alia M. Arab and Tarek A. Azeim and Teshreen M. Zeitoun and Wafaa A. Hewedy and Moemen A. Heiba and Iman S. Emara", title = "Is Curcumine Effect Comparable to 5- Aminosalicylic Acid or Budesonide on a Rat Model of Ulcerative Colitis Induced by Trinitrobenzene Sulfonic Acid?", abstract = "Inflammatory bowel disease (IBD) is a chronic
relapsing-remitting condition that afflicts millions of people
throughout the world and impairs their daily functions and quality of
life. Treatment of IBD depends largely on 5-aminosalicylic acid (5-
ASA) and corticosteroids. The present study aimed to clarify the
effects of 5-aminosalicylic acid, budesonide and currcumin on 90
male albino rats against trinitrobenzene sulfonic acid (TNB) induced
colitis. TNB was injected intrarectally to 50 rats. The other 40 rats
served as control groups. Both 5-ASA (in a dose of 120 mg/kg) and
budesonide (in a dose of 0.1 mg/kg) were administered daily for one
week whereas currcumin was injected intraperitonially (in a dose of
30 mg/kg daily) for 14 days after injection of either TNB in the
colitis rats (group B) or saline in control groups (group A). The study
included estimation of macroscopic score index, histological
examination of H&E stained sections of the colonic tissue,
biochemical estimation of myeloperoxidase (MPO), nitric oxide
(NO), and caspase-3 levels, in addition to studying the effect of tested
drugs on colonic motility. It was found that budesonide and curcumin
improved mucosal healing, reduced both NO production and caspase-
3 level. They had the best impact on the disturbed colonic motility in
TNBS-model of colitis.
", keywords = "Colitis, curcumin, nitric oxide.", volume = "7", number = "8", pages = "504-9", }
