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. 2014 Apr 15;7(5):2153-62.
eCollection 2014.

Somatostatin regulates tight junction proteins expression in colitis mice

Xiao Li  1 , Qian Wang  1 , Hua Xu  2 , Liping Tao  1 , Jing Lu  1 , Lin Cai  1 , Chunhui Wang  1
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VSports注册入口 - Somatostatin regulates tight junction proteins expression in colitis mice

Xiao Li et al. Int J Clin Exp Pathol. .

"VSports app下载" Abstract

Tight junction plays a critical role in intestinal defence. The alteration and perturbation of tight junction proteins could induce intestine barrier damage, and lead to the malabsorption of electrolytes and water. Previous studies had showed that colonic infection and inflammation could lead to the alteration of tight junction function, and somatostatin could protect intestinal epithelia. Thus, this study could explore that whether somatostatin could regulate tight junction in colitis mice. Colitis mice with diarrhea were induced by Citrobacter rodentium (CR) and Dextran sulfate sodium (DSS) VSports手机版. In CR infected model, cladudin-1 and claudin-3 expression significantly decreased compared with the control mice (P<0. 05); after octreotide treatment, claudin-1 and claudin-3 expression significantly increased compared with untreated CR infected mice (P<0. 05). In DSS colitis model, occludin and claudin-3 expression significantly decreased compared with the control mice (P<0. 05); and octreotide treatment could only significantly upregulate claudin-3 expression compared with untreated DSS colitis mice (P<0. 05). To testify our results in vivo, we repeated the models in caco-2 cells by exposed with enteropathogenic Escherichia coli (E. Coli) and Tumor necrosis factor α (TNF-α). The results in vitro were consistent with in vivo study. The results suggested that somatostatin play a role in intestinal barrier protection by modulating tight junction proteins expression. .

Keywords: IBD; Tight junction; claudins; infectious colitis; occludin; somatostatin. V体育安卓版.

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Figures

Figure 1
Figure 1
Diarrhea scores and somatostatin assay in CR infected mice and DSS colitis mice. Mice were infected with CR or fed with DSS water before octreotide treatment. Diarrhea scores were recorded and somatostatin was measured. CT: control group; CR: CR infected group; DSS: DSS colitis group; Oct: Octreotide. Data are presented as mean ± SE from three groups of mice (3 mice/group). *p < 0.05 for treatment mice (Oct) vs. CR mice (CR) or DSS mice (DSS); #p < 0.05 for CR mice (CR) and DSS mice vs. control mice (CT). A: Diarrheal score in CR infected mice. B: Diarrheal score in DSS colitis mice. C: Somatostatin levels in the proximal colon. D: Somatostatin level in the distal colon.
Figure 2
Figure 2
Effect of octreotide on claudin-1 and claudin-3 expression in CR infected mice. Colonic tissues were collected from control mice (CT), CR infected mice (CR) and octreotide treated mice (CR+Oct). Tissue lysate was used to detect claudin-1 and claudin-3 expression by western blot. Data are presented as mean ± SE from 3 groups of mice (3 mice/group). *p < 0.05 for CR mice (CR) vs. control mice (CT) and octreotide treated mice (Oct). A: The ratio of optical density of claudin-1 over GAPDH in the proximal colon. B: The ratio of optical density of claudin-1 over GAPDH in the distal colon. C: The ratio of optical density of claudin-3 over GAPDH in the proximal colon. D: The ratio of optical density of claudin-3 over GAPDH in the distal colon.
Figure 3
Figure 3
Effect of octreotide on occludin and claudin-3 expression in DSS colitis mice. Colonic tissues were collected from control mice (CT), DSS mice (DSS) and octrotide treated mice (DSS+Oct). Tissue lysate was used to detect occludin and claudin-3 expression by western blot. Tissue lysate was used to detect occludin and claudin-3 expression by western blot. Data are presented as mean ± SE from 3 groups of mice (3 mice/group). #p < 0.05 for DSS mice (DSS) and octreotide mice (Oct) vs. control mice; *p < 0.05 for DSS mice (DSS) vs. control mice (CT) and octreotide treated mice (Oct). A: The ratio of optical density of occludin over GAPDH in the proximal colon. B: The ratio of optical density of occludin over GAPDH in the distal colon. C: The ratio of optical density of claudin-3 over GAPDH in the proximal colon. D: The ratio of optical density of claudin-3 over GAPDH in the proximal colon.
Figure 4
Figure 4
Immunohistochemical assay of claudin-3 in mucosal epithelium in DSS colitis mice. Histological observation of colonic tissues from control mice (CT), DSS mice (DSS) and octrotide treated mice (Oct). Tissues were used for histological assay. A: H&E stain of mice colon tissues. B: Immunohistochemical staining shows Claudin-3 in yellow. While Claudin-3 is decreased in DSS mice colon, treatment with Oct restored Claudin-3 expression.
Figure 5
Figure 5
Effect of somatostatin on claudin-1 and claudin-3 expression in Caco-2 cells. Caco-2 cells were preincubated with 1×107 cfu/ml EPEC for 1 hour or 100 ng/ml TNF-α for 18 hours before adding 1 μM somatostatin. Cell lysate was used to detect claudin-1 and claudin-3 expression by western blot. Data are presented as Mean ± SE from 3 separate experiments. *p < 0.05 for EPEC or TNF-α treated cells vs. control cells and somatostatin treated cells. A: The ratio of optical density of claudin-3 over GAPDH in EPEC infected cells. B: The ratio of optical density of claudin-3 over GAPDH in TNF-α treated cells. C: The ratio of optical density of claudin-1 over GAPDH in EPEC infected cells.
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