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, 9 (4), 341-50

Sodium Arsenite Reduces Severity of Dextran Sulfate Sodium-Induced Ulcerative Colitis in Rats

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Sodium Arsenite Reduces Severity of Dextran Sulfate Sodium-Induced Ulcerative Colitis in Rats

Joshua J Malago et al. J Zhejiang Univ Sci B.

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.

Figures

Fig. 1
Fig. 1
Effect of sodium arsenite (SA) on clinical indices of colitis. Rats were treated with 5% dextran sulfate sodium (DSS) orally, SA (10 mg/kg, intraperitoneally) followed by DSS or SA alone. Values for control rats are also indicated but overlap with those of SA. (a) Cycle 1; (b) Cycle 2; (c) Cycle 3 Weight loss is in comparison to Day 1 of DSS administration
Fig. 1
Fig. 1
Effect of sodium arsenite (SA) on clinical indices of colitis. Rats were treated with 5% dextran sulfate sodium (DSS) orally, SA (10 mg/kg, intraperitoneally) followed by DSS or SA alone. Values for control rats are also indicated but overlap with those of SA. (a) Cycle 1; (b) Cycle 2; (c) Cycle 3 Weight loss is in comparison to Day 1 of DSS administration
Fig. 1
Fig. 1
Effect of sodium arsenite (SA) on clinical indices of colitis. Rats were treated with 5% dextran sulfate sodium (DSS) orally, SA (10 mg/kg, intraperitoneally) followed by DSS or SA alone. Values for control rats are also indicated but overlap with those of SA. (a) Cycle 1; (b) Cycle 2; (c) Cycle 3 Weight loss is in comparison to Day 1 of DSS administration
Fig. 2
Fig. 2
Effect of sodium arsenite (SA) administration on dextran sulfate sodium (DSS) colitis disease activity index. Rats were treated with 5% DSS orally, SA (10 mg/kg, intraperitoneally) followed by DSS or SA alone. Values for control rats are also indicated but overlap with those of SA. (a) Cycle 1; (b) Cycle 2; (c) Cycle 3 Disease activity index=(combined scores of weight loss (compared to Day 1 of the experiment), stool consistency and bleeding)/3; Results are expressed as the mean±SEM (n=8); * P<0.05, ** P<0.01, significantly different from DSS colitis group; # P<0.05, compared to those of DSS at the beginning of respective cycle
Fig. 2
Fig. 2
Effect of sodium arsenite (SA) administration on dextran sulfate sodium (DSS) colitis disease activity index. Rats were treated with 5% DSS orally, SA (10 mg/kg, intraperitoneally) followed by DSS or SA alone. Values for control rats are also indicated but overlap with those of SA. (a) Cycle 1; (b) Cycle 2; (c) Cycle 3 Disease activity index=(combined scores of weight loss (compared to Day 1 of the experiment), stool consistency and bleeding)/3; Results are expressed as the mean±SEM (n=8); * P<0.05, ** P<0.01, significantly different from DSS colitis group; # P<0.05, compared to those of DSS at the beginning of respective cycle
Fig. 2
Fig. 2
Effect of sodium arsenite (SA) administration on dextran sulfate sodium (DSS) colitis disease activity index. Rats were treated with 5% DSS orally, SA (10 mg/kg, intraperitoneally) followed by DSS or SA alone. Values for control rats are also indicated but overlap with those of SA. (a) Cycle 1; (b) Cycle 2; (c) Cycle 3 Disease activity index=(combined scores of weight loss (compared to Day 1 of the experiment), stool consistency and bleeding)/3; Results are expressed as the mean±SEM (n=8); * P<0.05, ** P<0.01, significantly different from DSS colitis group; # P<0.05, compared to those of DSS at the beginning of respective cycle
Fig. 3
Fig. 3
Histological sections of rat colon. (a), (b), (c) Rats were treated with 5% dextran sulfate sodium (DSS) orally; (d), (e), (f) Rats were treated with SA (10 mg/kg, intraperitoneally) followed by DSS; (g), (h), (i) Rats were treated with SA alone; (j) The control animal. (a), (d), (g) Cycle 1; (b), (e), (h) Cycle 2; (c), (f), (i) Cycle 3 Hematoxylin and eosin (H & E); 100× original magnification; Arrows indicating loss of epithelium; Each photo representing 8 animals (4 animals per treatment in duplicate experiments)
Fig. 3
Fig. 3
Histological sections of rat colon. (a), (b), (c) Rats were treated with 5% dextran sulfate sodium (DSS) orally; (d), (e), (f) Rats were treated with SA (10 mg/kg, intraperitoneally) followed by DSS; (g), (h), (i) Rats were treated with SA alone; (j) The control animal. (a), (d), (g) Cycle 1; (b), (e), (h) Cycle 2; (c), (f), (i) Cycle 3 Hematoxylin and eosin (H & E); 100× original magnification; Arrows indicating loss of epithelium; Each photo representing 8 animals (4 animals per treatment in duplicate experiments)
Fig. 3
Fig. 3
Histological sections of rat colon. (a), (b), (c) Rats were treated with 5% dextran sulfate sodium (DSS) orally; (d), (e), (f) Rats were treated with SA (10 mg/kg, intraperitoneally) followed by DSS; (g), (h), (i) Rats were treated with SA alone; (j) The control animal. (a), (d), (g) Cycle 1; (b), (e), (h) Cycle 2; (c), (f), (i) Cycle 3 Hematoxylin and eosin (H & E); 100× original magnification; Arrows indicating loss of epithelium; Each photo representing 8 animals (4 animals per treatment in duplicate experiments)
Fig. 3
Fig. 3
Histological sections of rat colon. (a), (b), (c) Rats were treated with 5% dextran sulfate sodium (DSS) orally; (d), (e), (f) Rats were treated with SA (10 mg/kg, intraperitoneally) followed by DSS; (g), (h), (i) Rats were treated with SA alone; (j) The control animal. (a), (d), (g) Cycle 1; (b), (e), (h) Cycle 2; (c), (f), (i) Cycle 3 Hematoxylin and eosin (H & E); 100× original magnification; Arrows indicating loss of epithelium; Each photo representing 8 animals (4 animals per treatment in duplicate experiments)
Fig. 3
Fig. 3
Histological sections of rat colon. (a), (b), (c) Rats were treated with 5% dextran sulfate sodium (DSS) orally; (d), (e), (f) Rats were treated with SA (10 mg/kg, intraperitoneally) followed by DSS; (g), (h), (i) Rats were treated with SA alone; (j) The control animal. (a), (d), (g) Cycle 1; (b), (e), (h) Cycle 2; (c), (f), (i) Cycle 3 Hematoxylin and eosin (H & E); 100× original magnification; Arrows indicating loss of epithelium; Each photo representing 8 animals (4 animals per treatment in duplicate experiments)
Fig. 3
Fig. 3
Histological sections of rat colon. (a), (b), (c) Rats were treated with 5% dextran sulfate sodium (DSS) orally; (d), (e), (f) Rats were treated with SA (10 mg/kg, intraperitoneally) followed by DSS; (g), (h), (i) Rats were treated with SA alone; (j) The control animal. (a), (d), (g) Cycle 1; (b), (e), (h) Cycle 2; (c), (f), (i) Cycle 3 Hematoxylin and eosin (H & E); 100× original magnification; Arrows indicating loss of epithelium; Each photo representing 8 animals (4 animals per treatment in duplicate experiments)
Fig. 3
Fig. 3
Histological sections of rat colon. (a), (b), (c) Rats were treated with 5% dextran sulfate sodium (DSS) orally; (d), (e), (f) Rats were treated with SA (10 mg/kg, intraperitoneally) followed by DSS; (g), (h), (i) Rats were treated with SA alone; (j) The control animal. (a), (d), (g) Cycle 1; (b), (e), (h) Cycle 2; (c), (f), (i) Cycle 3 Hematoxylin and eosin (H & E); 100× original magnification; Arrows indicating loss of epithelium; Each photo representing 8 animals (4 animals per treatment in duplicate experiments)
Fig. 3
Fig. 3
Histological sections of rat colon. (a), (b), (c) Rats were treated with 5% dextran sulfate sodium (DSS) orally; (d), (e), (f) Rats were treated with SA (10 mg/kg, intraperitoneally) followed by DSS; (g), (h), (i) Rats were treated with SA alone; (j) The control animal. (a), (d), (g) Cycle 1; (b), (e), (h) Cycle 2; (c), (f), (i) Cycle 3 Hematoxylin and eosin (H & E); 100× original magnification; Arrows indicating loss of epithelium; Each photo representing 8 animals (4 animals per treatment in duplicate experiments)
Fig. 3
Fig. 3
Histological sections of rat colon. (a), (b), (c) Rats were treated with 5% dextran sulfate sodium (DSS) orally; (d), (e), (f) Rats were treated with SA (10 mg/kg, intraperitoneally) followed by DSS; (g), (h), (i) Rats were treated with SA alone; (j) The control animal. (a), (d), (g) Cycle 1; (b), (e), (h) Cycle 2; (c), (f), (i) Cycle 3 Hematoxylin and eosin (H & E); 100× original magnification; Arrows indicating loss of epithelium; Each photo representing 8 animals (4 animals per treatment in duplicate experiments)
Fig. 3
Fig. 3
Histological sections of rat colon. (a), (b), (c) Rats were treated with 5% dextran sulfate sodium (DSS) orally; (d), (e), (f) Rats were treated with SA (10 mg/kg, intraperitoneally) followed by DSS; (g), (h), (i) Rats were treated with SA alone; (j) The control animal. (a), (d), (g) Cycle 1; (b), (e), (h) Cycle 2; (c), (f), (i) Cycle 3 Hematoxylin and eosin (H & E); 100× original magnification; Arrows indicating loss of epithelium; Each photo representing 8 animals (4 animals per treatment in duplicate experiments)
Fig. 4
Fig. 4
Histological scores of loss of epithelium (a), crypt damage (b), goblet cell depletion (c), and infiltration of inflammatory cells (d). Rats were treated with 5% dextran sulfate sodium (DSS) orally, SA (10 mg/kg, intraperitoneally) followed by DSS or SA alone Results are mean±SEM of at least 8 individual rats. * P<0.05, significantly different from DSS exposed rats
Fig. 4
Fig. 4
Histological scores of loss of epithelium (a), crypt damage (b), goblet cell depletion (c), and infiltration of inflammatory cells (d). Rats were treated with 5% dextran sulfate sodium (DSS) orally, SA (10 mg/kg, intraperitoneally) followed by DSS or SA alone Results are mean±SEM of at least 8 individual rats. * P<0.05, significantly different from DSS exposed rats
Fig. 4
Fig. 4
Histological scores of loss of epithelium (a), crypt damage (b), goblet cell depletion (c), and infiltration of inflammatory cells (d). Rats were treated with 5% dextran sulfate sodium (DSS) orally, SA (10 mg/kg, intraperitoneally) followed by DSS or SA alone Results are mean±SEM of at least 8 individual rats. * P<0.05, significantly different from DSS exposed rats
Fig. 4
Fig. 4
Histological scores of loss of epithelium (a), crypt damage (b), goblet cell depletion (c), and infiltration of inflammatory cells (d). Rats were treated with 5% dextran sulfate sodium (DSS) orally, SA (10 mg/kg, intraperitoneally) followed by DSS or SA alone Results are mean±SEM of at least 8 individual rats. * P<0.05, significantly different from DSS exposed rats

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