Role of β2-adrenoceptor-β-arrestin2-nuclear factor-κB signal transduction pathway and intervention effects of oxymatrine in ulcerative colitis

Heng Fan; Yi Liao; Qing Tang; Xiao-yan Chen; Li-juan Zhang; Xing-xing Liu; Min Zhong

doi:10.1007/s11655-012-1146-3

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Role of β2-adrenoceptor-β-arrestin2-nuclear factor-κB signal transduction pathway and intervention effects of oxymatrine in ulcerative colitis

Updated：2021-08-27

- Role of β2-adrenoceptor-β-arrestin2-nuclear factor-κB signal transduction pathway and intervention effects of oxymatrine in ulcerative colitis
- Chinese Journal of Integrative Medicine Vol. 18, Issue 7, Pages: 514-521(2012)
- Affiliations：
  
  Department of Integrated Chinese and Western Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Tecnology,Wuhan,China
- Author bio：
- Funds：
  
  Supported by the National Natural Science Foundation of China (No. 30772878)
- DOI：10.1007/s11655-012-1146-3
  CLC：
- Published：2012，
  
  Published Online：27 March 2013，
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Fan, H., Liao, Y., Tang, Q. et al. Role of β2-adrenoceptor-β-arrestin2-nuclear factor-κB signal transduction pathway and intervention effects of oxymatrine in ulcerative colitis., Chin. J. Integr. Med. 18, 514–521 (2012). https://doi.org/10.1007/s11655-012-1146-3

Heng Fan, Yi Liao, Qing Tang, et al. Role of β2-adrenoceptor-β-arrestin2-nuclear factor-κB signal transduction pathway and intervention effects of oxymatrine in ulcerative colitis. [J]. Chinese Journal of Integrative Medicine 18(7):514-521(2012)
Fan, H., Liao, Y., Tang, Q. et al. Role of β2-adrenoceptor-β-arrestin2-nuclear factor-κB signal transduction pathway and intervention effects of oxymatrine in ulcerative colitis., Chin. J. Integr. Med. 18, 514–521 (2012). https://doi.org/10.1007/s11655-012-1146-3 DOI：

Heng Fan, Yi Liao, Qing Tang, et al. Role of β2-adrenoceptor-β-arrestin2-nuclear factor-κB signal transduction pathway and intervention effects of oxymatrine in ulcerative colitis. [J]. Chinese Journal of Integrative Medicine 18(7):514-521(2012) DOI： 10.1007/s11655-012-1146-3.

摘要

To investigate the β2-adrenoceptor (β2AR)-β-arrestin2-nuclear factor-κB (NF-κB): signal transduction pathway and the intervention effects of oxymatrine in a rat model of ulcerative colitis. Forty SD rats were randomly divided into four groups

which included the normal control group

the model group

the mesalazine group and the oxymatrine treatment group

with 10 rats per group. Experimental colitis induced with trinitrobenzene sulfonic acid (TNBS) was established in each group except the normal control group. The rats in the oxymatrine treatment group were treated with intramuscular injection of oxymatrine 63 mg/(kg kg·d) for 15 days and the rats in the mesalazine group were treated with mesalazine solution 0.5 g/(kg kg·d) by gastric lavage for 15 days. The rats in the normal control group and model group were treated with 3 mL water by gastric lavage for 15 days. Diarrhea and bloody stool were carefully observed. Histological changes in colonic tissue were examined on day 7 in 2 rats per group that were randomly selected. The expression of β2AR

β-arrestin2 and NF-κB p65 in colon tissue and spleen lymphocytes were detected with immunohistochemistry and Western immunoblotting techniques on day 16 after fasting for 24 h. Six rats died of lavage with 2 each in the normal control

the model group and the mesalazine group; and were not included in the analysis. The rats in the model group suffered from: looser stool and bloody purulent stool after modeling. But in the oxymatrine and mesalazine groups

looser stool and bloody purulent stool reduced after treatment. And the colonic wall in the model group was thickened and the colon length shortened. The colon mucosa was congested in multiple areas with edema

erosion

superficial or linear ulcer and scar formation

while the intestinal mucosa injury reduced in the mesalazine and oxymatrine groups (P<0.01). In colonic mucosa and in spleen lymphocytes

compared with the normal control group

the expression of NF-κBp65 were significantly increased (P<0.01) in the model group while the expressions of β 2AR and β-arrestin2 were significantly decreased (P<0.01). Compared with the model group

the expression of NF-κ Bp65 was significantly decreased in the mesalazine group (P<0.01) and oxymatrine treatment group (P<0.01) while the expressions of β2AR and β-arrestin2 were significantly increased (P<0.01). There were no statistically significant differences in the expression of β2AR

β-arrestin2 and NF-κBp65 between the mesalazine group and oxymatrine group (P>0.05). The β2AR-β-arrestin2-NF-κB signal transduction pathway participated: in the pathologic course of ulcerative colitis. Oxymatrine attenuated ulcerative colitis through regulating the β2AR-β-arrestin2-NF-κB signal transduction pathway.

Abstract

which included the normal control group

the model group

the mesalazine group and the oxymatrine treatment group

erosion

superficial or linear ulcer and scar formation

while the intestinal mucosa injury reduced in the mesalazine and oxymatrine groups (P<0.01). In colonic mucosa and in spleen lymphocytes

compared with the normal control group

关键词

β2-adrenoceptorβ-arrestin2nuclear factor-κBsignal transductiontrinitrobenzene sulfonic acidUlcerative ColitisOxymatrine

Keywords

β2-adrenoceptorβ-arrestin2nuclear factor-κBsignal transductiontrinitrobenzene sulfonic acidUlcerative ColitisOxymatrine

references

Bouma G, Strober W. The immunological and genetic basis of inflammatory bowel disease. Nat Rev Immunol 2003; 3:521–533.

Xavier RJ, Podolsky DK. Unravelling the pathogenesis of inflammatory bowel disease. Nature 2007;448:427–434.

Neuman MG. Immune dysfunction in inflammatory bowel disease. Transl Res 2007;149:173–186.

Kucharzik T, Maaser C, Lügering A, Kagnoff M, Mayer L, Targan S, et al. Recent understanding of IBD pathogenesis: implications for future therapies. Inflamm Bowel Dis 2006;12:1068–1083.

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.

Chen F. Arresting NF-κB by β-arrestin2. Cell Death Differ 2004;11:1155–1156.

Gao H, Sun Y, Wu Y, Luan B, Wang Y, Qu B, et al. Identification of β-arrestin2 as a G Protein-Coupled Receptor-Stimulated Regulator of NF-κB pathways. Mol Cell 2004;14:303–317.

Fan H, Chen R, Shen L, Lu J, Xiong P, Shou Z, et al. Oxymatrine improves TNBS induced colitis in rats by inhibiting the expression of NF-κBp65. J Huazhong Univ Sci Technol Med Sci (Chin) 2008;28:415–420.

Zheng P, Niu FL, Liu WZ, Shi Y, Lu LG. Anti-inflammatory mechanism of oxymatrine in dextran sulfate sodiurn-induced colitis of rats. World J Gastroenterol 2005;11:4912–4915.

Lu JF, Fan H, Shen L, Shou ZhX, Zhuang X. Effects of Oxymatrine injection on expression of cytokines and nuclear factor-κB p65 in colonic intestinal mucosa of rats with experimental colitis. World J Gastroenterol 2008;16:896–899.

Morris GP, Beck PL, Herridge MS, Depew WT, Szewczuk MR, Wallace JL. Hapten-induced model of chronic inflammation and ulceration in the rat colon. Gastroenterology 1989;96:795–803.

Fan H, Qiu MY, Mei JJ, Shen GX, Liu SL, Chen R. Effects of four regulating-intestine prescriptions on pathology and ultrastructure of colon tissue in rats with ulcerative colitis. World J Gastroenterol 2005;11:4800–4806.

Fan H, Shen L, Tang Q, Xiong PC, Shou ZX, Liang L, et al. Effect of Wumeiwan on cytokine TNF-α, IL-6, IL-8, IL-10 and expression of NF-κB p65 of rats with ulcerative colitis. J Huazhong Univ Sci Technol Med Sci (Chin) 2009;29:650–654.

Fujino K, Takami Y, de la Fuente SG, Ludwig KA, Mantyh CR. Inhibition of the vanilloid receptor subtype-1 attenuates TNBS-colitis. J Gastrointest Surg 2004;8:842–847.

González R, Rodríguez S, Romay C. Anti-inflammatory activity of phycocyanin extract in acetic acid-induced colitis in rats. Parmacol Res 1999;39:55–59.

Shen GX, Zhou RL, eds. Experimental techniques of modern immunology. Wuhan: Hubei Science and Technology Press;2002:433–435.

Karin M, Yamamoto Y, Wang QM. The IKK NF-kappa B system: a treasure trove for drug development. Nat Rev Drug Discov 2004;3:17–26.

Tak PP, Firestein GS. NF-κB: a key role in inflammatory diseases. J Clin Invest 2001;107:7–11.

Karrasch T, Jobin C. NF-kappaB and the Intestine: friend or foe? Inflamm Bowel Dis 2008;14:114–124.

Witherow DS, Garrison TR, Miller WE, Lefkowitz RJ. Beta-Arrestin inhibits NF-kappaB activity by means of its interaction with the NF-kappaB inhibitor IkappaBalpha. Proc Natl Acad Sci USA 2004;101:8603–8607.

Wang Y, Tang Y, Teng L, Wu Y, Zhao X, Pei G. Association of beta-arrestin and TRAF6 negatively regulates Toll-like receptor-interleukin 1 receptor signaling. Nat Immunol 2006;7:139–147.

Abreu MT, Fukata M, Arditi M. TLR signaling in the Gut in health and disease. J Immunol 2005;174:4453–4460.

Kizaki T, Izawa T, Sakurai T, Haga S, Taniguchi N, Tajiri H, et al. Beta2-adrenergic receptor regulates Toll-like receptor-4-induced nuclear factor-kappaB activation through betaarrestin 2. Immunology 2008;124:348–356.

Kizaki T, Shirato K, Sakurai T, Ogasawara JE, Oh-ishi S, Matsuoka T, et al. Beta2-Adrenergic receptor regulate Toll-like receptor 4-induced late-phase NF-kaapaB activation. Mol Immunol 2009;46:1195–1203.

Zhang CQ, Feng J, Yan XN, Li WB, Hu G. Effects of Oxymatrine on the NF-kappa B expression of HaCaT cells. J Nanjing Med Univ (Chin) 2008;22:178–182.

Zhang CQ, Guo HL, Feng J, Yan XN, Li WB, Hu G. Effects of oxymatrine on expression of nuclear factor-kappa B and nitric oxide secretion in HaCat cells. J Clin Rehab Tissue Eng Res (Chin) 2008;12:3847–3852.

Liu Y, Zhang XJ, Yang CH, Fan HG. Oxymatrine protects rat brains against permanent focal ischemia and downregulates NF-κB expression. Brain Res 2009;1268:174–180.

Fan H, Zhuang X, Liang L, Liao Y, Tang Q. Therapeutic effects of colonic coated compound lightyellow sophora root capsules in patients with ulcerative colitis and mechanisms underlying such effects. World J Gastroenterol 2009:17:2429–2432.

Fan H, Shou ZX, Lu JF, Shen L, Yang SL, Chen R. Effect of compound Sophorae Flavescentis Jiechangrong Capsule on 11 cases of patients with ulcerative colitis. Chin J Integr Tradit West Med Digestion (Chin) 2007;15:60–61.

Liang L, Fan H, Tang Q, Chen XY. Effect of compound Sophorae Flavescentis Jiechangrong Capsule on 40 cases of patients with ulcerative colitis. Res Integr Tradit Chin West Med (Chin) 2010;2:7–10.

Fan H, Zhao J, Shen L, Tang Q, Shou ZX, Liang L, et al. Effect of compound Sophorae Flavescentis Jiechangrong Capsule on expression of NF-κBp65 and STAT6 in the intestinal mucosa of patients with ulcerative colitis. Frontiers Med Chin 2009;3:480–484.

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