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目的:了解肥大细胞(mast cell,MC)在人类原发性IgA肾病(IgAN)肾组织中的浸润及与肾小管间质损害程度、蛋白酶激活受体2(protease activated receptor-2 PAR-2)表达的关系,探寻肥大细胞在IgAN肾小管间质损害过程中的可能作用机制。方法:以35例IgAN肾活检石蜡包埋肾组织及5例肾肿瘤患者行肾切除的远离肿瘤部位的肾组织作为研究对象。根据Lee氏分级及Katafuchi半定量积分法分组。采用免疫组化法检测肾组织中MC和PAR-2的表达,分析它们之间及其与肾小管间质损害程度的相关性。所有数据均使用SPSS 13.0英文版统计软件进行分析。结果:(1)随着Lee氏分级等级的升高和肾小管间质损害程度的加重,MC数目和PAR-2的表达水平逐渐增加。(2)肾小管间质中MC、PAR-2的表达水平呈正相关(r=0.844,P<0.01)。肾小管间质中MC和PAR-2的表达水平均与肾小管间质病理积分呈正相关(r=0.948,0.840,P均<0.01)。结论:(1)MC浸润与原发性IgAN肾小管间质损害程度密切相关,MC可能是原发性IgAN肾小管间质损害过程的重要参与者。(2)类胰蛋白酶和PAR-2可能共同参与了原发性IgAN复杂的肾小管间质损害过程。
OBJECTIVE: To investigate the infiltration of mast cells (MCs) in renal tissues of human primary IgA nephropathy (IgAN) and their relationship with the damage of tubulointerstitial tissue. Protease activated receptor-2 (PAR-2) Expression of the relationship between mast cells to explore the possible mechanism of IgAN tubulointerstitial damage. Methods: 35 cases of renal tissue from paraffin-embedded renal tissue of IgAN and 5 cases of renal carcinoma underwent nephrectomy as the study area. According to Lee’s classification and Katafuchi semi-quantitative integration method grouping. Immunohistochemistry was used to detect the expression of MC and PAR-2 in renal tissue, and to analyze their correlation with the degree of tubulointerstitial damage. All data were analyzed using SPSS 13.0 English statistical software. Results: (1) The number of MC and the expression of PAR-2 gradually increased with the increase of Lee’s grade and the degree of tubulointerstitial damage. (2) The expressions of MC and PAR-2 in tubulointerstitial were positively correlated (r = 0.844, P <0.01). The expressions of MC and PAR-2 in tubulointerstitial were positively correlated with tubulointerstitial pathological scores (r = 0.948,0.840, P <0.01). Conclusion: (1) The infiltration of MC is closely related to the degree of tubulointerstitial injury of primary IgAN. MC may be an important participant in the process of primary tubulointerstitial damage of IgAN. (2) Tryptase and PAR-2 may participate in the complex process of primary tubulointerstitial damage of IgAN.