Role of DOR-β-arrestin1-Bcl2 signal transduction pathway and intervention effects of oxymatrine in ulcerative colitis
Role of DOR-β-arrestin1-Bcl2 signal transduction pathway and intervention effects of oxymatrine in ulcerative colitis
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DOI：
10.1007/s11596-014-1358-1
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发表时间：
2014-12-01
影响因子：
--
通讯作者：
Shou, Zhe-xing
中科院分区：
文献类型：
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作者：
Zhou, Pi-qi;Fan, Heng;Shou, Zhe-xing
本研究旨在探讨β-阿片受体(DOR)-β-arrestin1-Bcl2信号转导通路在溃疡性结肠炎(UC)发病机制中的作用及氧化苦参碱对UC的干预作用。将40只SD大鼠随机分为正常组、模型组、氧化苦参碱治疗组和美沙拉嗪治疗组，每组10只。模型组和治疗组大鼠结肠内注射三硝基苯磺酸建立大鼠UC模型。氧化苦参碱治疗组大鼠肌肉注射氧化苦参碱[63 mg/(kg中心点日)]15d，美沙拉嗪治疗组给予美沙拉秦溶液[0.5g/(kg中心点日)]灌胃15d。正常组和模型组灌胃3mL水，连续15d。第16天，禁食24小时后处死大鼠，取结肠组织。免疫组织化学和实时定量聚合酶链式反应(RT-PCR)分别检测结肠组织中DOR、β-arrestin1和Bcl2的表达水平。结果发现，模型组DOR、β-arrestin1和Bcl2蛋白及mRNA的表达水平均显著高于其他组(P<；0.05)。美沙拉秦治疗组和氧化苦参碱治疗组与模型组相比均明显降低(P<；0.05)。美沙拉秦治疗组和氧化苦参碱治疗组之间这些指标均无统计学差异(P>；0.05)。本研究提示DOR-β-arrestin1-Bcl2信号转导通路可能参与UC的发病机制。此外，氧化苦参碱通过调节DOR-β-arrestin1-Bcl2信号转导通路，延缓UC的发生发展。
This study was aimed to investigate the role of the delta-opioid receptor (DOR)-beta-arrestin1-Bcl-2 signal transduction pathway in the pathogenesis of ulcerative colitis (UC) and the intervention effects of oxymatrine on UC. Forty Sprague-Dawley rats were divided into normal group, model group, oxymatrine-treated group and mesalazine-treated group (n=10 each) at random. The rat UC model was established by intra-colonic injection of trinitrobenzene sulfonic acid in the model group and two treatment groups. The rats in oxymatrine-treated group were subjected to intramuscular injection of oxymatrine [63 mg/(kg center dot day)] for 15 days, and those in mesalazine-treated group given mesalazine solution [0.5 g/(kg center dot day)] by gastric lavage for the same days. Animals in normal group and model group were administered 3 mL water by gastric lavage for 15 days. On the 16th day, after fasting for 24 h, the rats were sacrificed for the removal of colon tissues. The expression levels of DOR, beta-arrestin1 and Bcl-2 were determined in colon tissues by immunohistochemistry and real-time quantitative polymerase chain reaction (RT-PCR), respectively. It was found that the expression levels of DOR, beta-arrestin1 and Bcl-2 protein and mRNA were significantly increased in the model group as compared with the other groups (P < 0.05). They were conspicuously decreased in both mesalazine-treated and oxymatrine-treated groups in contrast to the model group (P < 0.05). No statistically significant difference was noted in these indices between mesalazine- and oxymatrinetreated groups (P > 0.05). This study indicated that the DOR-beta-arrestin1-Bcl-2 signal transduction pathway may participate in the pathogenesis of UC. Moreover, oxymatrine can attenuate the development of UC by regulating the DOR-beta-arrestin1-Bcl-2 signal transduction pathway.