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Therapeutic effect of a hydroxynaphthoquinone fraction on dextran sulfate sodium-induced ulcerative colitis.
World J Gastroenterol. 2014 Nov 07; 20(41):15310-8.WJ

Abstract

AIM

To evaluate the therapeutic effect of hydroxynaphthoquinone mixture (HM) on dextran sulfate sodium (DSS)-induced colitis and explore the underlying mechanisms.

METHODS

BALB/c mice received 3.5% DSS for 6 d to induce ulcerative colitis. Groups of mice were orally administered HM 3.5, 7 and 14 mg/kg and mesalazine 200 mg/kg per day for 7 d. During the experiment, clinical signs and body weight, stool consistency and visible fecal blood were monitored and recorded daily. A disease activity index score was calculated for each animal. At the conclusion of the experiment, the colonic histopathological lesions were evaluated. Myeloperoxidase (MPO) activity and tumor necrosis factor-α (TNF-α) levels were determined. Protein expression levels of TNF-α, nuclear factor-κB (NF-κB) p65, inhibitor of κB (IκB) and phosphorylation of IκB (p-IκB) were analyzed by Western blot analysis.

RESULTS

Administration of 3.5% DSS for 6 d successfully induced acute colitis associated with soft stool, diarrhea, rectal bleeding, and colon shortening, as well as a loss of body weight. Administration of HM effectively attenuated the severity of colonic mucosa injury. For histopathological analysis, HM treatment improved histological alterations and lowered pathological scores compared with the DSS only group. This manifested as a reduction in the extent of colon injury and inflammatory cell infiltration, as well as the degree of mucosal destruction. In addition, HM at doses of 7 and 14 mg/kg significantly decreased MPO activity in colonic tissue (0.98 ± 0.22 U/g vs 1.32 ± 0.24 U/g, 0.89 ± 0.37 U/g vs 1.32 ± 0.24 U/g tissue, P < 0.05) and serum TNF-α levels (68.78 ± 7.34 ng/L vs 88.98 ± 17.79 ng/L, 64.13 ± 14.13 ng/L vs 88.98 ± 17.79 ng/L, P < 0.05). Furthermore, HM down-regulated the expression of TNF-α, NF-κB p65 and p-IκBα in colonic tissue while up-regulating IκBα protein expression. These results suggest that the significant anti-inflammatory effect of HM may be attributable to its inhibition of TNF-α production and NF-κB activation.

CONCLUSION

HM had a favorable therapeutic effect on DSS-induced ulcerative colitis, supporting its further development and clinical application in inflammatory bowel disease.

Authors+Show Affiliations

Zi-Liang Zhang, Ke Liu, College of Life Science, Jilin University, Changchun 130012, Jilin Province, China.Zi-Liang Zhang, Ke Liu, College of Life Science, Jilin University, Changchun 130012, Jilin Province, China.Zi-Liang Zhang, Ke Liu, College of Life Science, Jilin University, Changchun 130012, Jilin Province, China.Zi-Liang Zhang, Ke Liu, College of Life Science, Jilin University, Changchun 130012, Jilin Province, China.Zi-Liang Zhang, Ke Liu, College of Life Science, Jilin University, Changchun 130012, Jilin Province, China.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25386079

Citation

Zhang, Zi-Liang, et al. "Therapeutic Effect of a Hydroxynaphthoquinone Fraction On Dextran Sulfate Sodium-induced Ulcerative Colitis." World Journal of Gastroenterology, vol. 20, no. 41, 2014, pp. 15310-8.
Zhang ZL, Fan HY, Yang MY, et al. Therapeutic effect of a hydroxynaphthoquinone fraction on dextran sulfate sodium-induced ulcerative colitis. World J Gastroenterol. 2014;20(41):15310-8.
Zhang, Z. L., Fan, H. Y., Yang, M. Y., Zhang, Z. K., & Liu, K. (2014). Therapeutic effect of a hydroxynaphthoquinone fraction on dextran sulfate sodium-induced ulcerative colitis. World Journal of Gastroenterology, 20(41), 15310-8. https://doi.org/10.3748/wjg.v20.i41.15310
Zhang ZL, et al. Therapeutic Effect of a Hydroxynaphthoquinone Fraction On Dextran Sulfate Sodium-induced Ulcerative Colitis. World J Gastroenterol. 2014 Nov 7;20(41):15310-8. PubMed PMID: 25386079.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Therapeutic effect of a hydroxynaphthoquinone fraction on dextran sulfate sodium-induced ulcerative colitis. AU - Zhang,Zi-Liang, AU - Fan,Hua-Ying, AU - Yang,Ming-Yan, AU - Zhang,Zuo-Kai, AU - Liu,Ke, PY - 2014/05/20/received PY - 2014/06/21/revised PY - 2014/07/16/accepted PY - 2014/11/12/entrez PY - 2014/11/12/pubmed PY - 2015/8/11/medline KW - Arnebia euchroma (Royle) Johnst KW - Dextran sulfate sodium-induced ulcerative colitis KW - Hydroxynaphthoquinones KW - Inflammatory bowel disease KW - Nuclear factor-κB activation SP - 15310 EP - 8 JF - World journal of gastroenterology JO - World J. Gastroenterol. VL - 20 IS - 41 N2 - AIM: To evaluate the therapeutic effect of hydroxynaphthoquinone mixture (HM) on dextran sulfate sodium (DSS)-induced colitis and explore the underlying mechanisms. METHODS: BALB/c mice received 3.5% DSS for 6 d to induce ulcerative colitis. Groups of mice were orally administered HM 3.5, 7 and 14 mg/kg and mesalazine 200 mg/kg per day for 7 d. During the experiment, clinical signs and body weight, stool consistency and visible fecal blood were monitored and recorded daily. A disease activity index score was calculated for each animal. At the conclusion of the experiment, the colonic histopathological lesions were evaluated. Myeloperoxidase (MPO) activity and tumor necrosis factor-α (TNF-α) levels were determined. Protein expression levels of TNF-α, nuclear factor-κB (NF-κB) p65, inhibitor of κB (IκB) and phosphorylation of IκB (p-IκB) were analyzed by Western blot analysis. RESULTS: Administration of 3.5% DSS for 6 d successfully induced acute colitis associated with soft stool, diarrhea, rectal bleeding, and colon shortening, as well as a loss of body weight. Administration of HM effectively attenuated the severity of colonic mucosa injury. For histopathological analysis, HM treatment improved histological alterations and lowered pathological scores compared with the DSS only group. This manifested as a reduction in the extent of colon injury and inflammatory cell infiltration, as well as the degree of mucosal destruction. In addition, HM at doses of 7 and 14 mg/kg significantly decreased MPO activity in colonic tissue (0.98 ± 0.22 U/g vs 1.32 ± 0.24 U/g, 0.89 ± 0.37 U/g vs 1.32 ± 0.24 U/g tissue, P < 0.05) and serum TNF-α levels (68.78 ± 7.34 ng/L vs 88.98 ± 17.79 ng/L, 64.13 ± 14.13 ng/L vs 88.98 ± 17.79 ng/L, P < 0.05). Furthermore, HM down-regulated the expression of TNF-α, NF-κB p65 and p-IκBα in colonic tissue while up-regulating IκBα protein expression. These results suggest that the significant anti-inflammatory effect of HM may be attributable to its inhibition of TNF-α production and NF-κB activation. CONCLUSION: HM had a favorable therapeutic effect on DSS-induced ulcerative colitis, supporting its further development and clinical application in inflammatory bowel disease. SN - 2219-2840 UR - https://www.unboundmedicine.com/medline/citation/25386079/Therapeutic_effect_of_a_hydroxynaphthoquinone_fraction_on_dextran_sulfate_sodium_induced_ulcerative_colitis_ L2 - http://www.wjgnet.com/1007-9327/full/v20/i41/15310.htm DB - PRIME DP - Unbound Medicine ER -