FOLLOWUS
1. School of Pharmacy, Guangdong Medical College,Guangdong Province,Dongguan,China
2. School of Traditional Chinese Medicine, Southern Medical University,Guangzhou,China
纸质出版日期:2011,
网络出版日期:2011-8-9,
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Zhao, Wc., Song, Lj. & Deng, Hz. Protective effect of total alkaloids of Sophora alopecuroides on dextran sulfate sodium-induced chronic colitis., Chin. J. Integr. Med. 17, 616 (2011). https://doi.org/10.1007/s11655-011-0813-0
Wen-chang Zhao, Li-jun Song, Hong-zhu Deng. Protective effect of total alkaloids of Sophora alopecuroides on dextran sulfate sodium-induced chronic colitis[J]. Chinese Journal of Integrative Medicine, 2011,17(8):616-624.
Zhao, Wc., Song, Lj. & Deng, Hz. Protective effect of total alkaloids of Sophora alopecuroides on dextran sulfate sodium-induced chronic colitis., Chin. J. Integr. Med. 17, 616 (2011). https://doi.org/10.1007/s11655-011-0813-0 DOI:
Wen-chang Zhao, Li-jun Song, Hong-zhu Deng. Protective effect of total alkaloids of Sophora alopecuroides on dextran sulfate sodium-induced chronic colitis[J]. Chinese Journal of Integrative Medicine, 2011,17(8):616-624. DOI: 10.1007/s11655-011-0813-0.
To investigate the effect of total alkaloids of Sophora alopecuroides (TASA) on dextran sulfate sodium (DSS)-induced colitis in mice. Chronic experimental colitis was induced by administration of 4 cycles of 4% DSS. Fifty mice were randomly distributed into 4 groups (normal
DSS
DSS/high-dose TASA
and DSS/low-dose TASA groups) by a random number table with body weight stratification. Mice in the normal group (n=11) and DSS-induced colitis control group (n=15) received control treatment of 20 mL/kg distilled water; DSS plus TASA high- and low-dose groups (n=12 each) were treated with TASA solution (20 mL/kg) at the doses of 60 mg/kg and 30 mg/kg
respectively. The severity of colitis was assessed on the basis of clinical signs
colon length
and histology scores. Moreover
secretory immunoglobulin A (sIgA) and haptoglobin (HP) were analyzed by enzyme linked immunosorbent assay; intercellular adhesion molecule 1 (ICAM-1) and macrophage-migration inhibitory factor (MIF) gene expressions were analyzed by quantitative reverse transcriptase realtime polymerase chain reaction (qRT-PCR) using SYBA green I; and nuclear factor κ B (NF-κ B) expression and activation and p65 interaction with the promoter of ICAM-1 gene were assessed by Western blotting and chromatin immunoprecipitation assay. TASA administration significantly attenuated the damage and substantially reduced HP elevation and maintained the level of cecum sIgA. TASA inhibited the ICAM-1 gene expression and had no effect on MIF gene expression. Also
TASA was able to reduce phospho-I κ B α (p-I κ B α) protein expression; however
it had no effect on the activation of I κ B kinase α (IKK α) and inhibitor of NF-κ B α (I κ B α). Moreover
TASA inhibited the p65 recruitment to the ICAM-1 gene promoter. TASA had a protective effect on DSS-induced colitis. Such effect may be associated with its inhibition of NF-κ B activation and blockade of NF-κ B-regulated transcription activation of proinflammatory mediator gene.
To investigate the effect of total alkaloids of Sophora alopecuroides (TASA) on dextran sulfate sodium (DSS)-induced colitis in mice. Chronic experimental colitis was induced by administration of 4 cycles of 4% DSS. Fifty mice were randomly distributed into 4 groups (normal
DSS
DSS/high-dose TASA
and DSS/low-dose TASA groups) by a random number table with body weight stratification. Mice in the normal group (n=11) and DSS-induced colitis control group (n=15) received control treatment of 20 mL/kg distilled water; DSS plus TASA high- and low-dose groups (n=12 each) were treated with TASA solution (20 mL/kg) at the doses of 60 mg/kg and 30 mg/kg
respectively. The severity of colitis was assessed on the basis of clinical signs
colon length
and histology scores. Moreover
secretory immunoglobulin A (sIgA) and haptoglobin (HP) were analyzed by enzyme linked immunosorbent assay; intercellular adhesion molecule 1 (ICAM-1) and macrophage-migration inhibitory factor (MIF) gene expressions were analyzed by quantitative reverse transcriptase realtime polymerase chain reaction (qRT-PCR) using SYBA green I; and nuclear factor κ B (NF-κ B) expression and activation and p65 interaction with the promoter of ICAM-1 gene were assessed by Western blotting and chromatin immunoprecipitation assay. TASA administration significantly attenuated the damage and substantially reduced HP elevation and maintained the level of cecum sIgA. TASA inhibited the ICAM-1 gene expression and had no effect on MIF gene expression. Also
TASA was able to reduce phospho-I κ B α (p-I κ B α) protein expression; however
it had no effect on the activation of I κ B kinase α (IKK α) and inhibitor of NF-κ B α (I κ B α). Moreover
TASA inhibited the p65 recruitment to the ICAM-1 gene promoter. TASA had a protective effect on DSS-induced colitis. Such effect may be associated with its inhibition of NF-κ B activation and blockade of NF-κ B-regulated transcription activation of proinflammatory mediator gene.
total alkaloids of Sophora alopecuroidesdextran sulfate sodiumcolitisnuclear factor κ B signaltransduction pathway
total alkaloids of Sophora alopecuroidesdextran sulfate sodiumcolitisnuclear factor κ B signaltransduction pathway
Bouma G, Strober W. The immunological and genetic basis of inflammatory bowel disease. Nature 2003;3:521–534.
Macdonald TT, Monteleone G. Immunity, inflammation, and allergy in the gut. Science 2005;5717:1920–1925.
Podolsky DK. Inflammatory bowel disease. N Engl J Med 2002;6:417–430.
Sartor RB. Mechanisms of disease: pathogenesis of Crohn’s disease and ulcerative colitis. Nat Clin Pract Gastroenterol Hepatol 2006;3:390–407.
Atreya I, Atreya R, Neurath MF. NF-κB in inflammatory bowel disease. J Intern Med 2008;263:591–596.
Visekruna A, Joeris T, Seidel D, Kroesen A, Loddenkemper C, Zeitz M, et al. Proteasome-mediated degradation of IκBα and processing of p105 in Crohn’ disease and ulcerative colitis. J Clin Invest 2006; 12:3195–3203.
Han Y, Zhou Y, Liu Q. Antiendotoxic effects of Sophora alopecuroides L. J Chin Med Mater (Chin) 2006;10:1066–1069.
Mou XL, Wang WB, Ba H, Alkber H, Liao LX. A review on the progress in the chemical compounds and pharmacology of Sophora alopecuroides L. J Xinjiang Normal Univ (Natural Sci Ed, Chin) 2005;1:45–50.
Zhao WC, Song LJ, Deng HZ. Research on preparation of guar-based hydrophilic matrix tablets containing total alkaloids of Sophora alopecuroides and its in vitro sophoridine release. Chin J Exp Tradit Med Formul (Chin) 2010;6:1–5.
Chen JG, Deng HZ. Effects of total base of Sophora alopecuroides on expression of SOD, MDA, NO, MPO in rats with experimental colitis. J Chin Mater Med (Chin) 2006;4:323–325.
Zhao W, Song L, Deng H, Yao H. Hydration, erosion and release behavior of guar-based hydrophilic matrix tablets containing total alkaloids of Sophora alopecuroides. Drug Dev Ind Pharm 2009;5:594–602.
Zhou Y, Wang H, Liang L, Zhao WC, Chen Y, Deng HZ. Total alkaloids of Sophora alopecuroides increases the expression of CD4+ CD25+ Tregs and IL-10 in rats with experimental colitis. Am J Chin Med 2010;2:265–277.
Zhao WC, Song LJ, Deng HZ. Amelioration of dextran sulfate sodium-induced chronic colitis by sulfasalazine salicylazosulfapyridine via reducing NF-κB transcription factor p65 recruitment to ICAM-1 gene promoters. Yakugaku Zasshi 2010;9:1–11.
Zhao WC, Song LJ, Deng HZ. Effect of sophoridine on dextran sulfate sodium-induced colitis in C57BL/6 mice. J Asian Nat Prod Res 2010;12:925–933.
Borm MEA, Bouma G. Animal models of inflammatory bowel disease. Drug Discov Today Dis Models 2004;1:437–444.
Jurjus AR, Khoury NN, Reimund JM. Animal models of inflammatory bowel disease. J Pharmacol Toxicol Methods 2004;50:81–92.
Shteingart S, Rapoport M, Grodzovski I, Sabag O, Lichtenstein M, Eavri R, et al. Therapeutic potency of IL-2 caspase-3 targeted treatment in a murine experimental model of inflammatory bowel disease (IBD). Gut 2008;4:628–635.
Research Group of Guidance on GPT 3-1. Guidance on chronic toxicity testing in animals (rodent and nonrodent toxicity testing) for traditional Chinese medicine and naturally occurring drugs. 2005:3–16.
Lu YX, Lu JT, Chen MZ. Therapeutic effect of interleukin-10 on rat adjuvant arthritis. Chin Pharmacol Bull (Chin) 2000;16:103–107.
Melgar S, Karlsson A, Michaëlsson E. Acute colitis induced by dextran sulfate sodium progresses to chronicity in C57BL/6 but not in BALB/c mice: correlation between symptoms and inflammation. Am J Physiol Gastrointest Liver Physiol 2005;288:G1328–G1338.
Keith CT, Borisy AA, Stockwell BR. Multicomponent therapeutics for networked systems. Nat Rev Drug Discov 2005;4:71–78.
Mora JR, Iwata M, Eksteen B, Song SY, Junt T, Senman B, et al. Generation of gut-homing IgA-secreting B cells by intestinal dendritic cells. Science 2006;314:1157–1162.
Danese S, Semeraro S, Marini M, Roberto I, Armuzzi A, Papa A, et al. Adhesion molecules in inflammatory bowel disease: therapeutic implications for gut inflammation. Dig Liver Dis 2005;37:811–818.
Van Assche G, Rutgeerts P. Physiological basis for novel drug therapies used to treat the inflammatory bowel diseases. I. Immunology and therapeutic potential of antiadhesion molecule therapy in inflammatory bowel disease. Am J Physiol Gastrointest Liver Physiol 2005;288:G169–G174.
Roebuck KA, Finnegan A. Regulation of intercellular adhesion molecule-1 (CD54) gene expression. J Leukoc Biol 1999;66:876–889.
Morand EF. New therapeutic target in inflammatory disease: macrophage migration inhibitory factor. J Intern Med 2005;35:419–426.
Ohkawara T, Nishihira J, Takeda H, Asaka M, Sugiyama T. Pathophysiological roles of macrophage migration inhibitory factor in gastrointestinal, hepatic, and pancreatic disorders. J Gastroenterol 2005;40:117–122.
Mochizuki M, Hasegawa N. Therapeutic efficacy of pycnogenol in experimental inflammatory bowel diseases. Phytother Res 2005;12:1027–1028.
Xavier RJ, Podolsky DK. Unravelling the pathogenesis of inflammatory bowel disease. Nature 2007;448:427–434.
de Jong YP, Abadia-Molina AC, Satoskar AR, Clarke K, Rietdijk ST, Faubion WA, et al. Development of chronic colitis is dependent on the cytokine MIF. Nat Immunol 2001;11:1061–1066.
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