摘要
目的：
探讨埋线上巨虚”、“天枢”、“大肠俞”治疗大鼠实验性结肠炎的作用机制。
方法：
24只Sprague Dawley (SD)大鼠随机分为穴位埋线组、美沙拉嗪组、模型组、正常对照组4组,每组6只,除正常对照组未造模外,其余3组大鼠均采用TNBS造模诱导大鼠形成实验性结肠炎模型,穴位埋线组于“上巨虚”、“天枢”“大肠俞”处进行穴位埋线治疗,美沙拉嗪组予美沙拉嗪混悬液灌胃,模型组和正常组大鼠不设干预,正常饮食,第16d禁食24h后处死大鼠。治疗15d后观察大鼠的一般情况如腹泻、便血症状等,用免疫组化染色法观察大鼠结肠组织IL-17、Foxp3、β2AR、NF-κBp65的表达；用Western blot(?)去检测大鼠脾淋巴细胞β2AR和NF-κBp65蛋白的表达；用RT-PCR观察大鼠结肠组织STAT6mRNA的表达。
结果：
与正常对照组比较,模型组NF-κBp65、STAT6mRNA表达水平显著上升(P<0.01),β2AR表达水平显著下降(P<0.01),IL-17的表达也上升,Foxp3的表达也下降；与模型组比较,美沙拉嗪组NF-κBp65、STAT6mRNA表达水平显著下降(P<0.01),β2AR表达水平显著上升(P<0.01),IL-17的表达也下降,Foxp3的表达也上升；与模型组比较,穴位埋线组NF-κBp65、STAT6mRNA表达水平均显著下降(P<0.01),β2AR表达水平显著上升(P<0.01),IL-17的表达也下降,Foxp3的表达也上升。
结论：
模型大鼠中β2AR、Foxp3的表达下降,IL-17、NF-κBp65、STAT6mRNA的表达上升,是实验性结肠炎大鼠的重要致病机制,NF-κB/STAT6双信号转导通
路参与实验性结肠炎大鼠的发病过程,穴位埋线“上巨虚”、“天枢”、“大肠俞”可
以通过降低IL-17、NF-κBp65、STAT6mRNA的表达,减轻实验性结肠炎大鼠的
病理改变,从而发挥抗炎修复作用。
Objective:
To investigate the mechanisms of acupoint catgut embedding on the rats with experimental colitis.
Methods:
Twenty-four SD rats were randomly divided into a normal control group(NC), a model group (MO), a Mesalazine groups (ME) and an acupoint catgut embedding group (CI) with 6 rats in each group. The rats in Mesalazine group were given mesalazine through intragastriclly administration everyday and the rats in acupoint catgut embedding group were given catgut point-embedding therapy. The symptoms of changes in histopathology were detected 15 days after the treatment. Colonic histopathologic changes were observed by immunohistochemical staining and the expression of IL-17, Foxp3,β2AR, NF-KBp65 was observed by Immunohistochemistry. The protein expression ofβ2AR, NF-KBp65 was analyzed by western blot method and the expression of STAT6mRNA was detected by RT-PCR.
Results:
Compared with the control group, there was elevated expression of IL-17, NF-KBp65, STAT6mRNA (P<0.01),and decreased expression of Foxp3,P2AR (P< 0.01) in experimental UC rats.After experimental UC rats treated with mesalazine, the level of IL-17, NF-κBp65, STAT6mRNAwas significantly decreased (P<0.01) accompanied by significant up-regulation of Foxp3,βAR expression (P<0.01) in Mesalazine group.Compared with the model group, the level of IL-17, NF-κBp65, STAT6mRNA was also decreased(P<0.01) accompanied by significant up-regulation of Foxp3,β2AR (P<0.01) in acupoint catgut embedding group.
Conclusion:
The expression ofβ2AR, Foxp3 is decreased,and the expression of IL-17, NF-KBp65, and STAT6mRNA is increased, which is a possible pathogenesis of experimental UC rats.NF-κB/STAT6 double signal transduction pathways play an important role for pathogenic process of experimental UC in rats.Acupoint catgut embedding therapy can inhibit the expression of IL-17,NF-κBp65,STAT6mRNA to play anti-inflammatory role.
引文
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1. Morris G P, Beck P L, Herridge M S, et al. Hapten-induced model of chronic inflammation and ulceration in the rat colon[J].Castroenterology,1989, 96:795-803.
2.Cheng F, Li Q. Advance in catgut implantation at acupoints for treatment of ulcerative colitis. J Clin Acup Mox (Chin) 2004; 20(10):54-55.
3. Li HJ, Li GP, Li HY. Clinical observation on treatment of ulcerative colitis by catgut implantation at acupoints. Chin Acup-Mox (Chin) 2006; 26(4):261-263.
4.张光奇,向开维,杨孝芳,等.穴位埋线对实验性大鼠溃疡性结肠炎粘附分子CD44、CD54及白细胞介素2的影响[J].中国针灸,2002,22(11)：765-768.
5.Zhu Y, Yuan WJ, Bai XM. Influence of catgut implantation at acupoints on modulator proteins for apoptosis of lymphocytes in ulcerative colitis. J Tradit Chin Med (Chin) 2007; 48(6):526-528.
6.朱莹,袁伟建,姚红艳.穴位埋线对溃疡性结肠炎患者血清IL-22受体及T淋巴细胞亚群的影响[J].中国中西医结合杂志,2003,23(1)：58-59.
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11.Wallach D, Vorfolmeev E E, Malinin N L, et al. Tumor necrosis factor receptor and fas signaling mechanisms [J]. Annu Rev Immunol,1999,17:331-367.
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