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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

XLS stimulated enterocyte proliferation in DSS-treated rats. (a) Water + saline; (b) water + XLS; (c) DSS + saline; and (d) DSS + XLS (immunohistochemistry, ×40 and ×400 original magnification). (e) Cell proliferation was evaluated by LI, representative of the immunoreactivity of Ki-67 in colon sections. Numbers in brackets represent sample numbers of each group. **P < 0.01 versus water + saline, &&P < 0.01 versus water + saline, and $P < 0.05 versus DSS + XLS.
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fig6: XLS stimulated enterocyte proliferation in DSS-treated rats. (a) Water + saline; (b) water + XLS; (c) DSS + saline; and (d) DSS + XLS (immunohistochemistry, ×40 and ×400 original magnification). (e) Cell proliferation was evaluated by LI, representative of the immunoreactivity of Ki-67 in colon sections. Numbers in brackets represent sample numbers of each group. **P < 0.01 versus water + saline, &&P < 0.01 versus water + saline, and $P < 0.05 versus DSS + XLS.

Mentions: Ki-67, a nuclear protein expressed in all active phases of the cell cycle, is necessary for cell proliferation. To explore whether or not XLS could interfere with enterocyte proliferation, we evaluated the Ki-67 expression in colonic epithelium as a function of the LI. Ki-67 immunohistochemistry exhibited low expression in epithelial cells in the water + saline group (Figure 6(a)). In contrast, DSS treatment increased the Ki-67 expression as seen by comparing the water + saline and the DSS + saline groups (Figure 6(c)) (27 ± 2% in LI [N = 7] versus 43 ± 3% [N = 10], P < 0.01 in Figure 6(e)). Interestingly, XLS, as well, promoted the expression of Ki-67, as evidenced by the comparison between the water + saline and water + XLS groups (Figure 6(b)) (27 ± 2% in LI [N = 7] versus 40 ± 3% [N = 8], P < 0.01 in Figure 6(e)). The expression in the DSS + XLS group was even greater than that in the DSS + saline group (Figure 6(d)) (43 ± 3% in LI [N = 10] versus 50 ± 2% [N = 9], P = 0.19), although the difference was not statistically significant (Figure 6(e)). These data indicate that XLS stimulates enterocyte proliferation in DSS-induced colitis (Figure 6(d)).


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)

XLS stimulated enterocyte proliferation in DSS-treated rats. (a) Water + saline; (b) water + XLS; (c) DSS + saline; and (d) DSS + XLS (immunohistochemistry, ×40 and ×400 original magnification). (e) Cell proliferation was evaluated by LI, representative of the immunoreactivity of Ki-67 in colon sections. Numbers in brackets represent sample numbers of each group. **P < 0.01 versus water + saline, &&P < 0.01 versus water + saline, and $P < 0.05 versus DSS + XLS.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig6: XLS stimulated enterocyte proliferation in DSS-treated rats. (a) Water + saline; (b) water + XLS; (c) DSS + saline; and (d) DSS + XLS (immunohistochemistry, ×40 and ×400 original magnification). (e) Cell proliferation was evaluated by LI, representative of the immunoreactivity of Ki-67 in colon sections. Numbers in brackets represent sample numbers of each group. **P < 0.01 versus water + saline, &&P < 0.01 versus water + saline, and $P < 0.05 versus DSS + XLS.
Mentions: Ki-67, a nuclear protein expressed in all active phases of the cell cycle, is necessary for cell proliferation. To explore whether or not XLS could interfere with enterocyte proliferation, we evaluated the Ki-67 expression in colonic epithelium as a function of the LI. Ki-67 immunohistochemistry exhibited low expression in epithelial cells in the water + saline group (Figure 6(a)). In contrast, DSS treatment increased the Ki-67 expression as seen by comparing the water + saline and the DSS + saline groups (Figure 6(c)) (27 ± 2% in LI [N = 7] versus 43 ± 3% [N = 10], P < 0.01 in Figure 6(e)). Interestingly, XLS, as well, promoted the expression of Ki-67, as evidenced by the comparison between the water + saline and water + XLS groups (Figure 6(b)) (27 ± 2% in LI [N = 7] versus 40 ± 3% [N = 8], P < 0.01 in Figure 6(e)). The expression in the DSS + XLS group was even greater than that in the DSS + saline group (Figure 6(d)) (43 ± 3% in LI [N = 10] versus 50 ± 2% [N = 9], P = 0.19), although the difference was not statistically significant (Figure 6(e)). These data indicate that XLS stimulates enterocyte proliferation in DSS-induced colitis (Figure 6(d)).

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