Kalopanaxsaponin B Ameliorates TNBS-Induced Colitis in Mice
The stem-bark of Kalopanax pictus (KP, family Araliaceae), of which main constituent is kalopanaxsaponin B, has been used for asthma, rhinitis, and arthritis in Chinese traditional medicine. To clarify anticolitic effect of KP, we examined anti-inflammatory effect of KP extract and kalopanaxsaponin...
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| Published in | Biomolecules & therapeutics Vol. 20; no. 5; pp. 457 - 462 |
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| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Korea (South)
The Korean Society of Applied Pharmacology
01.09.2012
한국응용약물학회 |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1976-9148 2005-4483 2005-4483 |
| DOI | 10.4062/biomolther.2012.20.5.457 |
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| Abstract | The stem-bark of Kalopanax pictus (KP, family Araliaceae), of which main constituent is kalopanaxsaponin B, has been used for asthma, rhinitis, and arthritis in Chinese traditional medicine. To clarify anticolitic effect of KP, we examined anti-inflammatory effect of KP extract and kalopanaxsaponin B in lipopolysaccharide (LPS)-stimulated peritoneal macrophage and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitic mice. Of KP extracts, KP BuOH-soluble fraction most potently inhibited LPS-induced IL-1β, IL-6 and TNF-α expression, as well as NF-κB activation. However, KP BuOH fraction increased IL-10, an anti-inflammatory cytokine. KP BuOH fraction also inhibited colon shortening and myeloperoxidase activity in TNBS-induced colitic mice. KP BuOH fraction also potently inhibited the expression of the pro-inflammatory cytokines, IL-1β, IL-6 and TNF-α as well as the activation of NF-κB. Kalopanaxsaponin B, a main constituent of KP, inhibited TNBS-induced colonic inflammation, including colon shortening, and TNBS-increased myeloperoxidase activity pro-inflammatory cytokine expression and NF-κB activation in mice. Based on these findings, KP, particularly its main constituent, kalopanaxsaponin B, may ameliorate colitis by inhibiting NF-κB pathway. |
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| AbstractList | The stem-bark of Kalopanax pictus (KP, family Araliaceae), of which main constituent is kalopanaxsaponin B, has been used for asthma, rhinitis, and arthritis in Chinese traditional medicine. To clarify anticolitic effect of KP, we examined anti-inflammatory effect of KP extract and kalopanaxsaponin B in lipopolysaccharide (LPS)-stimulated peritoneal macrophage and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitic mice. Of KP extracts, KP BuOH-soluble fraction most potently inhibited LPS-induced IL-1b, IL-6 and TNF-a expression, as well as NF-κB activation. However, KP BuOH fraction increased IL-10, an anti-inflammatory cytokine. KP BuOH fraction also inhibited colon shortening and myeloperoxidase activity in TNBS-induced colitic mice. KP BuOH fraction also potently inhibited the expression of the pro-inflammatory cytokines, IL-1b, IL-6, and TNF-a as well as the activation of NF-κB. Kalopanaxsaponin B, a main constituent of KP, inhibited TNBS-induced colonic inflammation, including colon shortening,and TNBS-increased myeloperoxidase activity pro-inflammatory cytokine expression and NF-κB activation in mice. Based on these findings, KP, particularly its main constituent, kalopanaxsaponin B, may ameliorate colitis by inhibiting NF-κB pathway. KCI Citation Count: 9 The stem-bark of Kalopanax pictus (KP, family Araliaceae), of which main constituent is kalopanaxsaponin B, has been used for asthma, rhinitis, and arthritis in Chinese traditional medicine. To clarify anticolitic effect of KP, we examined anti-inflammatory effect of KP extract and kalopanaxsaponin B in lipopolysaccharide (LPS)-stimulated peritoneal macrophage and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitic mice. Of KP extracts, KP BuOH-soluble fraction most potently inhibited LPS-induced IL-1β, IL-6 and TNF-α expression, as well as NF-κB activation. However, KP BuOH fraction increased IL-10, an anti-inflammatory cytokine. KP BuOH fraction also inhibited colon shortening and myeloperoxidase activity in TNBS-induced colitic mice. KP BuOH fraction also potently inhibited the expression of the pro-inflammatory cytokines, IL-1β, IL-6 and TNF-α as well as the activation of NF-κB. Kalopanaxsaponin B, a main constituent of KP, inhibited TNBS-induced colonic inflammation, including colon shortening, and TNBS-increased myeloperoxidase activity pro-inflammatory cytokine expression and NF-κB activation in mice. Based on these findings, KP, particularly its main constituent, kalopanaxsaponin B, may ameliorate colitis by inhibiting NF-κB pathway.The stem-bark of Kalopanax pictus (KP, family Araliaceae), of which main constituent is kalopanaxsaponin B, has been used for asthma, rhinitis, and arthritis in Chinese traditional medicine. To clarify anticolitic effect of KP, we examined anti-inflammatory effect of KP extract and kalopanaxsaponin B in lipopolysaccharide (LPS)-stimulated peritoneal macrophage and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitic mice. Of KP extracts, KP BuOH-soluble fraction most potently inhibited LPS-induced IL-1β, IL-6 and TNF-α expression, as well as NF-κB activation. However, KP BuOH fraction increased IL-10, an anti-inflammatory cytokine. KP BuOH fraction also inhibited colon shortening and myeloperoxidase activity in TNBS-induced colitic mice. KP BuOH fraction also potently inhibited the expression of the pro-inflammatory cytokines, IL-1β, IL-6 and TNF-α as well as the activation of NF-κB. Kalopanaxsaponin B, a main constituent of KP, inhibited TNBS-induced colonic inflammation, including colon shortening, and TNBS-increased myeloperoxidase activity pro-inflammatory cytokine expression and NF-κB activation in mice. Based on these findings, KP, particularly its main constituent, kalopanaxsaponin B, may ameliorate colitis by inhibiting NF-κB pathway. The stem-bark of Kalopanax pictus (KP, family Araliaceae), of which main constituent is kalopanaxsaponin B, has been used for asthma, rhinitis, and arthritis in Chinese traditional medicine. To clarify anticolitic effect of KP, we examined anti-inflammatory effect of KP extract and kalopanaxsaponin B in lipopolysaccharide (LPS)-stimulated peritoneal macrophage and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitic mice. Of KP extracts, KP BuOH-soluble fraction most potently inhibited LPS-induced IL-1β, IL-6 and TNF-α expression, as well as NF-κB activation. However, KP BuOH fraction increased IL-10, an anti-inflammatory cytokine. KP BuOH fraction also inhibited colon shortening and myeloperoxidase activity in TNBS-induced colitic mice. KP BuOH fraction also potently inhibited the expression of the pro-inflammatory cytokines, IL-1β, IL-6 and TNF-α as well as the activation of NF-κB. Kalopanaxsaponin B, a main constituent of KP, inhibited TNBS-induced colonic inflammation, including colon shortening, and TNBS-increased myeloperoxidase activity pro-inflammatory cytokine expression and NF-κB activation in mice. Based on these findings, KP, particularly its main constituent, kalopanaxsaponin B, may ameliorate colitis by inhibiting NF-κB pathway. |
| Author | Joh, Eun-Ha Jeong, Jun-Ju Han, Myung-Joo Kim, Dong-Hyun Jang, Se-Eun |
| AuthorAffiliation | 2 Department of Food and Nutrition, Kyung Hee University, Seoul 130-701, Republic of Korea 1 Department of Life and Nanopharmaceutical Sciences and Department of Pharmaceutical Science, Kyung Hee University, Seoul 130-701, Republic of Korea |
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| CitedBy_id | crossref_primary_10_1155_2014_352371 crossref_primary_10_1016_j_jconrel_2020_01_047 crossref_primary_10_2174_1573406416666200227122849 crossref_primary_10_1016_j_fitote_2023_105561 crossref_primary_10_1007_s10787_021_00813_y crossref_primary_10_3389_fnut_2022_898417 crossref_primary_10_1016_j_hermed_2021_100504 crossref_primary_10_1002_jssc_201400771 |
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| References_xml | – ident: OOOMB4_2012_v20n5_457_006 doi: 10.1016/S0378-8741(01)00383-X – ident: OOOMB4_2012_v20n5_457_007 doi: 10.1074/jbc.274.16.10689 – ident: OOOMB4_2012_v20n5_457_012 doi: 10.1002/ptr.3596 – ident: OOOMB4_2012_v20n5_457_018 doi: 10.1007/BF03216748 – ident: OOOMB4_2012_v20n5_457_019 doi: 10.1055/s-2001-11516 – ident: OOOMB4_2012_v20n5_457_008 doi: 10.1038/sj.bjp.0702879 – volume: 165 start-page: 818 year: 2002 ident: OOOMB4_2012_v20n5_457_015 publication-title: Am. J. Respir. Crit. Care Med. doi: 10.1164/ajrccm.165.6.2101049 – ident: OOOMB4_2012_v20n5_457_017 doi: 10.1016/j.ejphar.2010.08.046 – ident: OOOMB4_2012_v20n5_457_004 doi: 10.1016/0003-2697(76)90527-3 – ident: OOOMB4_2012_v20n5_457_013 doi: 10.1172/JCI117676 – ident: OOOMB4_2012_v20n5_457_002 doi: 10.1016/j.bpg.2003.12.002 – ident: OOOMB4_2012_v20n5_457_010 doi: 10.1111/j.1476-5381.2010.01195.x – ident: OOOMB4_2012_v20n5_457_009 doi: 10.1016/S0891-5520(05)70078-7 – volume: 100 start-page: 1180 year: 1991 ident: OOOMB4_2012_v20n5_457_020 publication-title: Gastroenterology doi: 10.1016/0016-5085(91)70002-F – ident: OOOMB4_2012_v20n5_457_022 doi: 10.1016/S0140-6736(02)07284-7 – ident: OOOMB4_2012_v20n5_457_005 doi: 10.1128/IAI.68.12.7010-7017.2000 – ident: OOOMB4_2012_v20n5_457_014 doi: 10.1248/bpb.25.472 – ident: OOOMB4_2012_v20n5_457_021 doi: 10.1023/A:1026634229934 – ident: OOOMB4_2012_v20n5_457_003 doi: 10.1016/0306-3623(95)02141-8 – ident: OOOMB4_2012_v20n5_457_016 doi: 10.1186/1476-9255-7-7 – ident: OOOMB4_2012_v20n5_457_001 doi: 10.1038/75068 – ident: OOOMB4_2012_v20n5_457_011 doi: 10.1016/j.bcp.2011.05.003 – reference: 11809204 - Lancet. 2002 Jan 5;359(9300):62-9 – reference: 21198552 - Br J Pharmacol. 2011 Apr;162(8):1731-42 – reference: 20181058 - J Inflamm (Lond). 2010 Feb 01;7:7 – reference: 2013367 - Gastroenterology. 1991 May;100(5 Pt 1):1180-6 – reference: 20828550 - Eur J Pharmacol. 2010 Dec 1;648(1-3):162-70 – reference: 7814646 - J Clin Invest. 1995 Jan;95(1):55-65 – reference: 8909977 - Gen Pharmacol. 1996 Sep;27(6):973-7 – reference: 11301855 - Planta Med. 2001 Mar;67(2):118-21 – reference: 11995927 - Biol Pharm Bull. 2002 Apr;25(4):472-6 – reference: 11801382 - J Ethnopharmacol. 2002 Feb;79(2):199-204 – reference: 21928370 - Phytother Res. 2012 Apr;26(4):546-51 – reference: 11897650 - Am J Respir Crit Care Med. 2002 Mar 15;165(6):818-23 – reference: 10340170 - Infect Dis Clin North Am. 1999 Jun;13(2):341-53, vii – reference: 10802717 - Nat Med. 2000 May;6(5):583-8 – reference: 10556937 - Br J Pharmacol. 1999 Nov;128(5):999-1010 – reference: 9875510 - Arch Pharm Res. 1998 Feb;21(1):24-9 – reference: 942051 - Anal Biochem. 1976 May 7;72:248-54 – reference: 10196138 - J Biol Chem. 1999 Apr 16;274(16):10689-92 – reference: 15157821 - Best Pract Res Clin Gastroenterol. 2004 Jun;18(3):463-79 – reference: 21600888 - Biochem Pharmacol. 2011 Aug 1;82(3):278-86 – reference: 11083826 - Infect Immun. 2000 Dec;68(12):7010-7 – reference: 10080162 - Dig Dis Sci. 1999 Mar;44(3):637-42 |
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| Title | Kalopanaxsaponin B Ameliorates TNBS-Induced Colitis in Mice |
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