Wnt5a在慢性根尖周炎病损中的表达及临床意义
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摘要
目的 :检测慢性根尖周炎根尖病损区Wnt5a的水平与细胞定位,探讨Wnt5a与炎症细胞浸润程度的关系,以及Wnt5a在慢性根尖周炎发展中的作用及意义。方法:选取10例慢性根尖周炎牙作为实验组,根据根尖区组织的H-E染色,依炎症细胞浸润程度将病例组分为轻中度组、重度组。5例因正畸需要而拔除的健康牙作为对照组。采用实时定量PCR(real-time PCR,RT-PCR)从m RNA水平检测样本Wnt5a的表达;免疫组织化学法检测样本中Wnt5a蛋白的表达,应用图像分析软件检测Wnt5a蛋白表达水平,分析Wnt5a表达高低与炎症程度的关系。采用SPSS13.0软件包对数据进行统计学分析。结果:Wnt5a在实验组与对照组均有表达,实验组中Wnt5a m RNA表达水平显著高于对照组(P<0.05)。免疫组织化学结果显示,重度炎症组Wnt5a的表达水平显著高于对照组(P<0.01);轻中度组Wnt5a的表达水平显著高于对照组(P<0.05);重度炎症组中Wnt5a的表达水平显著高于轻中度炎症组(P<0.05)。结论:Wnt5a与慢性根尖周炎的炎症程度相关,可能参与了病变的始动过程,推测Wnt5a在慢性根尖周炎的发生、发展中起着一定作用。
PURPOSE: To detect the expression of Wnt5 a in lesions of chronic apical periodontitis and determine the relationship between expression of Wnt5 a and inflammation degree. METHODS: Ten patients with chronic apical periodontitis and 5 healthy controls were enrolled in this study. According to the inflammatory cell infiltration, the specimens were divided into 2 groups: severe inflammation group and mild inflammation group. The expression of Wnt5 a was measured by real- time PCR( RT- PCR) and immunohistochemical analysis in the lesions of chronic apical periodontitis. The amount of Wnt5 expression was assayed and compared in different inflammation levels. Statistical analysis was performed using SPSS 13.0 software package. RESULTS: Wnt5 a was detected in both groups. Expression of Wnt5 a m RNA in patients were significantly higher than the controls(P<0.05). According to inflammation level, the positive expression rate of Wnt5 a in severe inflammation group was significantly higher than the controls( P <0.01), and Wnt5 a positive expression in mild inflammation group was also significantly higher than the controls( P<0.05). The expression of Wnt5 a was significantly different between severe inflammation group and mild inflammation group( P <0.05).CONCLUSIONS: The expression of Wnt5 a increases as the severity of tissue inflammation increases, which indicates that Wnt5 a plays an important role in the development of chronic apical periodontitis.
PURPOSE: To detect the expression of Wnt5 a in lesions of chronic apical periodontitis and determine the relationship between expression of Wnt5 a and inflammation degree. METHODS: Ten patients with chronic apical periodontitis and 5 healthy controls were enrolled in this study. According to the inflammatory cell infiltration, the specimens were divided into 2 groups: severe inflammation group and mild inflammation group. The expression of Wnt5 a was measured by real- time PCR( RT- PCR) and immunohistochemical analysis in the lesions of chronic apical periodontitis. The amount of Wnt5 expression was assayed and compared in different inflammation levels. Statistical analysis was performed using SPSS 13.0 software package. RESULTS: Wnt5 a was detected in both groups. Expression of Wnt5 a m RNA in patients were significantly higher than the controls(P<0.05). According to inflammation level, the positive expression rate of Wnt5 a in severe inflammation group was significantly higher than the controls( P <0.01), and Wnt5 a positive expression in mild inflammation group was also significantly higher than the controls( P<0.05). The expression of Wnt5 a was significantly different between severe inflammation group and mild inflammation group( P <0.05).CONCLUSIONS: The expression of Wnt5 a increases as the severity of tissue inflammation increases, which indicates that Wnt5 a plays an important role in the development of chronic apical periodontitis.
引文
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[18]Min KJ,Cho KH,Kwon TK.The effect of oxidized low density lipoprotein(ox LDL)-induced heme oxygenase-1 on LPS-induced inflammation in RAW 264.7 macrophage cells[J].Cell Signal,2012,24(6):1215-1221.
[2]Katoh M,Katoh M.STAT3-induced WNT5A signaling loop in embryonic stem cells,adult normal tissues,chronic persistent inflammation,rheumatoid arthritis and cancer[J].Int J Mol Med,2007,19(2):273-278.
[3]Malgor R,Bhatt PM,Connolly BA,et al.Wnt5a,TLR2 and TLR4are elevated in advanced human atherosclerotic lesions[J].Inflamm Res,2014,63(4):277-285.
[4]胡蓉,廖端芳,覃丽.Wnt5a与动脉粥样硬化的研究进展[J].现代生物医学进展,2012,12(17):3354-3357.
[5]Nanbara H,Wara-aswapati N,Nagasawa T,et al.Modulation of Wnt5a expression by periodontopathic bacteria[J].PLOS One,2012,7(4):e34434.
[6]Riedemann NC,Guo RF,Ward PA.Novel strategies for the treatment of sepsis[J].Nat Med,2003,9(5):517-524.
[7]Kabashima H,Nagata K,Maeda K,et al.Involvement of substance P,mast cells,TNF-alpha and ICAM-1 in the infiltration of inflammatory cells in human periapical granulomas[J].J Oral Pathol Med,2002,31(3):175-180.
[8]施庆颜,靳华,曾靖华,等.白细胞介素1β和白细胞介素17在根尖周病组织肥大细胞上的表达[J].中国病理生理杂志,2014,30(9):1666-1671.
[9]郎小英,李颂.RORγT在人根尖肉芽肿和根尖囊肿中的表达及意义[J].上海口腔医学,2014,23(4):465-471.
[10]Hansson GK,Libby P.The immune response in atherosclerosis:a double-edged sword[J].Nat Rev Immunol,2006,6(7):508-519.
[11]Pereira C,Schaer DJ,Bachli EB,et al.Wnt5A/Ca MKll signaling contributes to the inflammatory response of macrophages and is a target for the antiinflammatory action of activated protein C and interleukin-10[J].Arterioscler Thrombo Vasc Biol,2008,28(3):504-510.
[12]Ataoǐg lu T,Ungor M,Serpek B,et al.Interleukin-1 beta and tumor necrosis factor-alpha levels in periapical exudates[J].Int Endod J,2002,35(2):181-185.
[13]Danin J,Linder LE,Lundqvist G,et al.Tumor necrosis factoralpha and transforming growth factor-beta1 in chronic periapical lesions[J].Oral Surg Oral Med Oral Pathol Oral Radiol Endod,2000,90(4):514-517.
[14]赵战芝,姜志胜,卜梓斌,等.ox HDL3、ox LDL诱导THP-1单核源性巨噬细胞表达IL-1β、IL-6、HLA-DR、CD86[J].中国免疫学杂志,2008,24(4):365-373.
[15]赵玉雪,赵丽娟.白细胞介素-1及其与牙周病的关系[J].中国实用口腔科杂志,2012,5(6):379-382.
[16]Catalán V,Gómez-Ambrosi J,Rodríguez A,et al.Activation of noncanonical Wnt signaling through WNT5A in visceral adipose tissue of obese subjects is related to inflammation[J].J Clin Endocrinol Metab,2014,99(8):E1407-1417.
[17]Zhao Y,Wang CL,Li RM,et al.Wnt5a promotes inflammatory responses via nuclear factorκB(NF-κB)and mitogen-activated protein kinase(MAPK)pathways in human dental pulp cells[J].J Biol Chem,2014,289(30):21028-21039.
[18]Min KJ,Cho KH,Kwon TK.The effect of oxidized low density lipoprotein(ox LDL)-induced heme oxygenase-1 on LPS-induced inflammation in RAW 264.7 macrophage cells[J].Cell Signal,2012,24(6):1215-1221.