Gallic Acid Inhibits STAT3 Phosphorylation and Alleviates DDS-induced Colitis via Regulating Cytokine Production
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Signal transducer and activator of transcription 3 (STAT3) is associated with various human diseases, such as cancer, auto-immune disease, and intestinal inflammation. The limited and inadequate effect of standard approaches for treating inflammatory bowel disease (IBD) has prompted to develop alternative anti-colitis agents through inhibition of STAT3. Here, we show that gallic acid (GA), a 3,4,5-trihydroxybenzoic acid, markedly reduced phosphorylation of STAT3. Among the derivatives of benzoic acids, GA showed significant inhibition on STAT3 phosphorylation. In addition, GA ameliorated the dextran sodium sulfate (DSS)-induced acute colitis as determined by the measurement of symptomatic and histological indices. The suppression of DSS-induced acute colitis by GA treatment may be related to the regulation of cytokines and growth factors. Furthermore, GA inhibited phosphorylation of STAT3 in the colon tissue of DSS-treated mice. These findings may be useful in comprehending the molecular action of GA on STAT3 phosphorylation and provide novel insights into the potential application of GA in the treatment of STAT3-related inflammatory disease, such as IBD.
Abstract
Signal transducer and activator of transcription 3 (STAT3) is associated with various human diseases, such as cancer, auto-immune disease, and intestinal inflammation. The limited and inadequate effect of standard approaches for treating inflammatory bowel disease (IBD) has prompted to develop alternative anti-colitis agents through inhibition of STAT3. Here, we show that gallic acid (GA), a 3,4,5-trihydroxybenzoic acid, markedly reduced phosphorylation of STAT3. Among the derivatives of benzoic acids, GA showed significant inhibition on STAT3 phosphorylation. In addition, GA ameliorated the dextran sodium sulfate (DSS)-induced acute colitis as determined by the measurement of symptomatic and histological indices. The suppression of DSS-induced acute colitis by GA treatment may be related to the regulation of cytokines and growth factors. Furthermore, GA inhibited phosphorylation of STAT3 in the colon tissue of DSS-treated mice. These findings may be useful in comprehending the molecular action of GA on STAT3 phosphorylation and provide novel insights into the potential application of GA in the treatment of STAT3-related inflammatory disease, such as IBD.
참고문헌 (55)
- Atreya, R., "Novel signal transduction pathways: analysis of STAT-3 and Rac-1 signaling in inflammatory bowel disease", Annals of the New York Academy of Sciences, 1072, pp.98~113 (2006)
- Milner, J. D., "Early-onset lymphoproliferation and autoimmunity caused by germline STAT3 gain-of-function mutations", Blood, 125, pp.591~599 (2015)
- Li, Y., "New insights into the role of STAT3 in IBD", Inflammatory bowel diseases, 18, pp.1177~1183 (2012)
- Li, N., "The unholy trinity: inflammation, cytokines, and STAT3 shape the cancer microenvironment", Cancer cell, 19, pp.429~431 (2011)
- Chassaing, B., "Dextran sulfate sodium (DSS)-induced colitis in mice", Current protocols in immunology, 104, pp.Unit 15~ (2014)
- Ordas, I., "Ulcerative colitis", Lancet, 380, pp.1606~1619 (2012)
- Alex, P., "Distinct cytokine patterns identified from multiplex profiles of murine DSS and TNBS-induced colitis", Inflammatory bowel diseases, 15, pp.341~352 (2009)
- Neurath, M. F., "Cytokines in inflammatory bowel disease", Nature reviews Immunology, 14, pp.329~342 (2014)
- Coskun, M., "Involvement of JAK", STAT signaling in the pathogenesis of inflammatory bowel disease, 2013, pp.76, 1~8
- Plevy, S., "A STAT need for human immunologic studies to understand inflammatory bowel disease", The American journal of gastroenterology, 100, pp.73~74 (2005)
- Adams, S. M., "Ulcerative colitis", American family physician, 87, pp.699~705 (2013)
- Nielsen, O. H., "New strategies for treatment of inflammatory bowel disease", Frontiers in medicine, 1, pp.3~ (2014)
- Atreya, R., "New therapeutic strategies for treatment of inflammatory bowel disease", Mucosal immunology, 1, pp.175~182 (2008)
- Sandborn, W. J., "Tofacitinib, an oral Janus kinase inhibitor, in active ulcerative colitis", The New England journal of medicine, 367, pp.616~624 (2012)
- Panes, J., "Randomized trial of tofacitinib in active ulcerative colitis: analysis of efficacy based on patient-reported outcomes", BMC gastroenterology, 15, pp.14~ (2015)
- Jayamani, J., "Gallic acid, one of the components in many plant tissues, is a potential inhibitor for insulin amyloid fibril formation", European journal of medicinal chemistry, 85, pp.352~358 (2014)
- Wang, K., "Investigation of gallic acid induced anticancer effect in human breast carcinoma MCF-7 cells", Journal of biochemical and molecular toxicology, 28, pp.387~393 (2014)
- Bravo, H. R., "1,4-benzoxazin-3-one, 2-benzoxazolinone and gallic acid from Calceolaria thyrsiflora Graham and their antibacterial activity. Zeitschrift fur Naturforschung C", Journal of biosciences, 60, pp.389~393 (2005)
- Kim, Y. J., "Antimelanogenic and antioxidant properties of gallic acid", Biological & pharmaceutical bulletin, 30, pp.1052~1055 (2007)
- Zhao, B., "Gallic acid reduces cell viability, proliferation, invasion and angiogenesis in human cervical cancer cells", Oncology letters, 6, pp.1749~1755 (2013)
- Hsiang, C. Y., "Toona sinensis and its major bioactive compound gallic acid inhibit LPS-induced inflammation in nuclear factor-kappaB transgenic mice as evaluated by in vivo bioluminescence imaging", Food chemistry, 136, pp.426~434 (2013)
- Ukil, A., "Protection from experimental colitis by theaflavin-3,3'-digallate correlates with inhibition of IKK and NF-kappaB activation", British journal of pharmacology, 149, pp.121~131 (2006)
- Jang, S. E., "Penta-O-galloyl-beta-D-glucose ameliorates inflammation by inhibiting MyD88", NF-kappaB and MyD88, British journal of pharmacology, pp.2013, 170[DOI]
- Xiao, H. T., "Inhibitory effect of the gallotannin corilagin on dextran sulfate sodium-induced murine ulcerative colitis", Journal of natural products, 76, pp.2120~2125 (2013)
- Abboud, P. A., "Therapeutic effect of epigallocatechin-3-gallate in a mouse model of colitis", European journal of pharmacology, 579, pp.411~417 (2008)
- Wang, Y., "Mechanism of the inhibition of the STAT3 signaling pathway by EGCG", Oncology reports, 30, pp.2691~2696 (2013)
- Lee, H. J., "Oral administration of penta-O-galloyl-beta-D-glucose suppresses triple-negative breast cancer xenograft growth and metastasis in strong association with JAK1-STAT3 inhibition", Carcinogenesis, 32, pp.804~811 (2011)
- Hu, H., "Penta-1,2,3,4,6-O-galloyl-beta-D-glucose induces p53 and inhibits STAT3 in prostate cancer cells in vitro and suppresses prostate xenograft tumor growth in vivo", Molecular cancer therapeutics, 7, pp.2681~2691 (2008)
- Shin, J. S., "Anti-inflammatory effect of a standardized triterpenoid-rich fraction isolated from Rubus coreanus on dextran sodium sulfate-induced acute colitis in mice and LPS-induced macrophages", Journal of ethnopharmacology, 158(Pt A), pp.291~300 (2014)
- Lin, L., "A novel small molecule inhibits STAT3 phosphorylation and DNA binding activity and exhibits potent growth suppressive activity in human cancer cells", Molecular cancer, 9, pp.217~ (2010)
- Axelsson, L. G., "Dextran sulfate sodium (DSS) induced experimental colitis in immunodeficient mice: effects in CD4(+) -cell depleted, athymic and NK-cell depleted SCID mice", Inflammation research : official journal of the European Histamine Research Society, 45, pp.181~191 (1996)
- Bantel, H., "TNF Antagonists in IBD: Novel Antiinflammatory Mechanisms Beyond Cytokine Inhibition", Inflammatory bowel diseases, 19, pp.E51~E52 (2013)
- Bersudsky, M., "Non-redundant properties of IL-1alpha and IL-1beta during acute colon inflammation in mice", Gut, 63, pp.598~609 (2014)
- Sandor, Z., "Altered angiogenic balance in ulcerative colitis: a key to impaired healing?", Biochemical and biophysical research communications, 350, pp.147~150 (2006)
- Toptygina, A. P., "Cytokine profile in children with inflammatory bowel disease", Biochemistry Biokhimiia, 79, pp.1371~1375 (2014)
- Fukuda, A., "Stat3 and MMP7 contribute to pancreatic ductal adenocarcinoma initiation and progression", Cancer cell, 19, pp.441~455 (2011)
- Rahimi, R., "Induction of clinical response and remission of inflammatory bowel disease by use of herbal medicines:A meta-analysis", World Journal of Gastroenterology (2013)
- Han, J., "How to achieve deep remission in treatment of inflammatory bowel disease", Journal of Traditional Chinese Medicine (2013)
- 이상욱, "해조가 2,4,6-trinitrobenzene-sulfonic acid로 유발된 염증성 장질환 동물모델에 미치는 영향", 대한한방내과학회지, 31(2), pp.224~241 (2010), 대한한방내과학회
- Ling, X. H., "Treatment of inflammatory bowel disease with Chinese drugs administered by both oral intake and retention enema", Chin J Integr Med, 16, pp.222~228 (2010)
- Lu, S. W., "Molecular mechanisms involved in the treatment of inflammatory bowel disease by Pulsatilla decoction", Chinese journal of applied physiology, 27, pp.106~109 (2011)
- You, Y., "Effect and Mechanism of Shenling Baizhu San on the Murine Model of Inflammatory Bowel Disease Induced by Dextran Sodium Sulfate in Mice", Chinese Journal of Experimental Traditional Medical Formulae, 18, pp.136~140 (2012)
- Qian, W., "Effect of Purslane Polysaccharide on Ulcerative Colitis Associated Colorectal Cancer and IL-6", STAT3 Pathway, 2013, pp.8, 1256~1260
- Iraha, A., "Fucoidan enhances intestinal barrier function by upregulating the expression of claudin-1", World Journal of Gastroenterology (2013)
- Kumar, V. S., "Naringin ameliorates acetic acid induced colitis through modulation of endogenous oxido-nitrosative balance and DNA damage in rats", Journal of Biomedical Research, 28 (2014)
- Rajasekaran, S.A., "Therapeutic potential of curcumin in gastrointestinal diseases", World Journal of Gastrointestinal Pathophysiology (2011)
- Chuan-zi, D., "Thinking on Functional Mechanism of Acupuncture for Inflammatory Bowel Diseases Based on Metabolomics", Journal of Acupuncture and Tuina Science (2014)
- Schneider, A., "Acupuncture treatment in gastrointestinal diseases: A systematic review", World Journal of Gastroenterology (2007)
- Piberger, H., "Bilberries and their anthocyanins ameliorate experimental colitis", Molecular nutrition & food research, 55, pp.1724~1729 (2011)
- Liu, L., "Curcumin ameliorates dextran sulfate sodium-induced experimental colitis by blocking STAT3 signaling pathway", International immunopharmacology, 17, pp.314~320 (2013)
- Wang, X. J., "The natural plant product sophocarpine ameliorates dextran sodium sulfate-induced colitis in mice by regulating cytokine balance", International journal of colorectal disease, 27, pp.575~581 (2012)
- Anthoni, C., "Mechanisms underlying the anti-inflammatory actions of boswellic acid derivatives in experimental colitis", American journal of physiology Gastrointestinal and liver physiology, 290, pp.G1131~G1137 (2006)
- Khanavi, M., "On the benefit of galls of Quercus brantii Lindl. in murine colitis: the role of free gallic acid", Archives of medical science : AMS, 10, pp.1225~1234 (2014)
- Pandurangan, A. K., "Gallic acid suppresses inflammation in dextran sodium sulfate-induced colitis in mice: Possible mechanisms", International immunopharmacology, 28, pp.1034~1043 (2015)
- Pandurangan, A. K., "Gallic acid attenuates dextran sulfate sodium-induced experimental colitis in BALB", c mice, 2015, pp.9, 3923~3934