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Xilei san ameliorates experimental colitis in rats by selectively degrading proinflammatory mediators and promoting mucosal repair.

Hao Y, Nagase K, Hori K, Wang S, Kogure Y, Fukunaga K, Kashiwamura S, Yamamoto S, Nakamura S, Li J, Miwa H, Noguchi K, Dai Y - Evid Based Complement Alternat Med (2014)

Bottom Line: Intrarectal administration of XLS attenuated the DSS-induced colitis, as evidenced by a reduction in both the histological damage score and myeloperoxidase activity.It also decreased the levels of proinflammatory cytokines, but increased the mucosal repair-related cytokines.These results suggest that XLS attenuates DSS-induced colitis by degrading proinflammatory mediators and promoting mucosal repair.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacy, School of Pharmacy, Hyogo University of Health Sciences, 1-3-6 Minatojima, Chuo-ku, Kobe, Hyogo 650-8530, Japan ; Division of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan.

ABSTRACT
Xilei san (XLS), a herbal preparation widely used in China for erosive and ulcerative diseases, has been shown to be effective in ulcerative colitis (UC). The present experiments were conducted to assess its efficacy and determine its mechanism of action in a rat model that resembles human UC. The model was induced by adding 4% dextran sulfate sodium (DSS) to the rats' drinking water for 7 days. XLS was administered daily by retention enema from day 2 to day 7; the rats were sacrificed on day 8. The colon tissues were obtained for further experiments. A histological damage score and the activity of tissue myeloperoxidase were used to evaluate the severity of the colitis. The colonic cytokine levels were detected in a suspension array, and epithelial proliferation was assessed using Ki-67 immunohistochemistry. Intrarectal administration of XLS attenuated the DSS-induced colitis, as evidenced by a reduction in both the histological damage score and myeloperoxidase activity. It also decreased the levels of proinflammatory cytokines, but increased the mucosal repair-related cytokines. In addition, the epithelial Ki-67 expression was upregulated by XLS. These results suggest that XLS attenuates DSS-induced colitis by degrading proinflammatory mediators and promoting mucosal repair. XLS could be a potential topical treatment for human UC.

No MeSH data available.


Related in: MedlinePlus

In rats, XLS upregulated colonic mucosal repair-related cytokine expression of (a) VEGF and (b) MIP-3α. Numbers in brackets represent sample numbers of each group. **P < 0.01 versus water + saline, *P < 0.05 versus water + saline, #P < 0.05 versus DSS + saline, &&P < 0.01 versus water + saline, and $$P < 0.01 versus DSS + XLS.
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fig5: In rats, XLS upregulated colonic mucosal repair-related cytokine expression of (a) VEGF and (b) MIP-3α. Numbers in brackets represent sample numbers of each group. **P < 0.01 versus water + saline, *P < 0.05 versus water + saline, #P < 0.05 versus DSS + saline, &&P < 0.01 versus water + saline, and $$P < 0.01 versus DSS + XLS.

Mentions: VEGF is a cytokine that promotes angiogenesis and MIP-3α functions in epithelial migration and mucosal barrier repair. Treatment with DSS reduced colonic VEGF (Figure 5(a)) and MIP-3α (Figure 5(b)) levels, as seen in the comparison between the assays for these moieties in the DSS + saline and water + saline groups (57.95 ± 14.20 pg/mg protein [N = 9] versus 147.42 ± 12.66 [N = 10], P < 0.01 for VEGF, and 511.64 ± 124.53 pg/mg protein [N = 9] versus 1781.36 ± 364.39 [N = 10], P < 0.05 for MIP-3α resp.), while XLS treatment significantly prevented that degradation, as evidenced by comparing the values obtained from the DSS + XLS and DSS + saline groups (117.75 ± 12.71 pg/mg protein [N = 10] versus 57.95 ± 14.20 [N = 9], P < 0.05 for VEGF, and 1358.20 ± 147.28 pg/mg protein [N = 10] versus 511.64 ± 124.53 [N = 9], P < 0.05 for MIP-3α, resp.). Furthermore, XLS treatment upregulated the MIP-3α expression in normal rats, as seen in the comparison of the MIP-3α from the water + XLS and the water + saline groups (3668.15 ± 265.42 pg/mg protein [N = 9] versus 1781.36 ± 364.39 [N = 10], P < 0.01) (Figure 5(b)).


Xilei san ameliorates experimental colitis in rats by selectively degrading proinflammatory mediators and promoting mucosal repair.

Hao Y, Nagase K, Hori K, Wang S, Kogure Y, Fukunaga K, Kashiwamura S, Yamamoto S, Nakamura S, Li J, Miwa H, Noguchi K, Dai Y - Evid Based Complement Alternat Med (2014)

In rats, XLS upregulated colonic mucosal repair-related cytokine expression of (a) VEGF and (b) MIP-3α. Numbers in brackets represent sample numbers of each group. **P < 0.01 versus water + saline, *P < 0.05 versus water + saline, #P < 0.05 versus DSS + saline, &&P < 0.01 versus water + saline, and $$P < 0.01 versus DSS + XLS.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig5: In rats, XLS upregulated colonic mucosal repair-related cytokine expression of (a) VEGF and (b) MIP-3α. Numbers in brackets represent sample numbers of each group. **P < 0.01 versus water + saline, *P < 0.05 versus water + saline, #P < 0.05 versus DSS + saline, &&P < 0.01 versus water + saline, and $$P < 0.01 versus DSS + XLS.
Mentions: VEGF is a cytokine that promotes angiogenesis and MIP-3α functions in epithelial migration and mucosal barrier repair. Treatment with DSS reduced colonic VEGF (Figure 5(a)) and MIP-3α (Figure 5(b)) levels, as seen in the comparison between the assays for these moieties in the DSS + saline and water + saline groups (57.95 ± 14.20 pg/mg protein [N = 9] versus 147.42 ± 12.66 [N = 10], P < 0.01 for VEGF, and 511.64 ± 124.53 pg/mg protein [N = 9] versus 1781.36 ± 364.39 [N = 10], P < 0.05 for MIP-3α resp.), while XLS treatment significantly prevented that degradation, as evidenced by comparing the values obtained from the DSS + XLS and DSS + saline groups (117.75 ± 12.71 pg/mg protein [N = 10] versus 57.95 ± 14.20 [N = 9], P < 0.05 for VEGF, and 1358.20 ± 147.28 pg/mg protein [N = 10] versus 511.64 ± 124.53 [N = 9], P < 0.05 for MIP-3α, resp.). Furthermore, XLS treatment upregulated the MIP-3α expression in normal rats, as seen in the comparison of the MIP-3α from the water + XLS and the water + saline groups (3668.15 ± 265.42 pg/mg protein [N = 9] versus 1781.36 ± 364.39 [N = 10], P < 0.01) (Figure 5(b)).

Bottom Line: Intrarectal administration of XLS attenuated the DSS-induced colitis, as evidenced by a reduction in both the histological damage score and myeloperoxidase activity.It also decreased the levels of proinflammatory cytokines, but increased the mucosal repair-related cytokines.These results suggest that XLS attenuates DSS-induced colitis by degrading proinflammatory mediators and promoting mucosal repair.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacy, School of Pharmacy, Hyogo University of Health Sciences, 1-3-6 Minatojima, Chuo-ku, Kobe, Hyogo 650-8530, Japan ; Division of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan.

ABSTRACT
Xilei san (XLS), a herbal preparation widely used in China for erosive and ulcerative diseases, has been shown to be effective in ulcerative colitis (UC). The present experiments were conducted to assess its efficacy and determine its mechanism of action in a rat model that resembles human UC. The model was induced by adding 4% dextran sulfate sodium (DSS) to the rats' drinking water for 7 days. XLS was administered daily by retention enema from day 2 to day 7; the rats were sacrificed on day 8. The colon tissues were obtained for further experiments. A histological damage score and the activity of tissue myeloperoxidase were used to evaluate the severity of the colitis. The colonic cytokine levels were detected in a suspension array, and epithelial proliferation was assessed using Ki-67 immunohistochemistry. Intrarectal administration of XLS attenuated the DSS-induced colitis, as evidenced by a reduction in both the histological damage score and myeloperoxidase activity. It also decreased the levels of proinflammatory cytokines, but increased the mucosal repair-related cytokines. In addition, the epithelial Ki-67 expression was upregulated by XLS. These results suggest that XLS attenuates DSS-induced colitis by degrading proinflammatory mediators and promoting mucosal repair. XLS could be a potential topical treatment for human UC.

No MeSH data available.


Related in: MedlinePlus