| IgA患者肾组织IL-37水平变化的研究 |
| 投稿时间：2018-01-10 修订日期：2018-01-30 点此下载全文 |
| 引用本文：陈志,刘云启,潘立平,金林.IgA患者肾组织IL-37水平变化的研究[J].医学研究杂志,2018,47(11):193-198,175 |
| DOI：
10.11969/j.issn.1673-548X.2018.11.043 |
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| 中文摘要:目的 通过检测IgA肾病不同程度肾纤维化患者肾组织IL-37、STAT3的表达，初步探讨IL-37在肾组织的表达情况及其与肾间质纤维化程度以及临床特征之间的相关关系。方法 根据肾纤维化的程度将37例IgA肾病患者分为实验组，5例肾脏良性肿瘤切除后远离肿瘤部位的肾组织作为对照组。实时定量PCR检测各组肾组织IL-37以及STAT3基因的表达，免疫组化检测各组肾组织IL-37及STAT3蛋白的表达，各组间进行比较，同时进行相关性分析。结果 正常肾组织IL-37存在初始表达，与对照组比较，实验组肾组织IL-37表达明显升高（P<0.05），但随着病变程度的加重，IL-37的表达反而下降。免疫组化检测结果显示，与对照组比较，实验组STAT3表达明显增加，且组间比较差异均有统计学意义（P<0.05）。IgA肾病患者肾组织IL-37表达量与肾间质纤维化程度呈负相关（r=-0.433，P=0.007）；STAT3的表达量与肾间质纤维化程度呈正相关（r=0.499，P=0.001）；实验组IL-37的表达量与STAT3呈负相关（r=-0.348，P=0.035）；IL-37的表达水平与患者24h尿蛋白定量呈负相关（P<0.05），而与性别、年龄、血肌酐、尿素氮、血浆白蛋白、炎细胞浸润以及临床分期无关（P>0.05）。结论 IgA肾病患者，随着肾脏病变程度的加重，炎性因子的释放刺激IL-37的表达增加，可能参与抑制过度的炎性反应，保护肾组织，本研究提示这种抗炎作用并不是无限制的。IL-37作为一种炎性保护因子，其变化的水平在一定程度上可提示肾脏病变的严重程度，或可成为肾脏纤维化治疗的新靶点。 |
| 中文关键词:IgA肾病 IL-37 STAT3 |
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| Exploratory Study on the IL-37 Changes in the Nephridial Tissue of IgA Nephrosis |
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| Abstract:Objective To discusse the expression status of IL-37 in the nephridial tissue, by checking the IL-37 and STAT3 expression of the nephridial tissue of patients suffered from renal fibrosis of different degrees, as well as its relevant relations with the renal interstitium fibrosis degree and the clinical features. Methods We set the 37 IgA nephrotic patients into the experimental group, and the nephridial tissue far from the tumor section in 5 cases of renal benign tumor after resection as the control group. After that, we made real-time quantitative PCR detection on the expression of IL-37 and STAT3 gene of the nephridial tissue in each group, and made the immunohistochemical detection on the expression of IL-37 and STAT3 of nephridial tissue in each group. Then, we conducted comparison between different groups as well as the correlation analysis. Results There was the primary expresson of IL-37 for normal nephridial tissue. Compared with the control group, the IL-37 expression of nephridial tissue in the experimental group rose up obviously (P<0.05). However, as the pathological degree was deteriorating, the expression of IL-37 was reducing. The immunocytochemistry showed that: compared with the control group, the STAT3 expression of the experimental group increased significantly. The difference derived from the comparison between groups had statistical significance (P<0.05). There was negative correlation between the IL-37 expression quantity with the fibrosis degree of renal interstitium (r=-0.433,P=0.007).The STAT3 expression quantity of nephridial tissue presentsed positive correlation with the fibrosis degree of renal interstitium (r=0.499,P=0.001). The expression quantity of IL-37 in the experimental group showed negative correlation with STAT3 (r=-0.348,P=0.035). The expression level of IL-37 was negative correlation with the 24-hour urine protein of patients (P<0.05), but didn'n have relation with the gender, age, serum creatinine, usea nitrogen, plasma albumin, Inflammatory cell infiltration or clinical stages (P>0.05). Conclusion For patients suffered from IgA nephrosis, with the deterioration of the pathological degree of kidney, the release of inflammatory factors trigger more IL-37 expression which might be involved in the inflammatory reaction of over-inhibition and protect the nephridial tissue. This experiment reminds us that such an anti-inflammatory action is not unlimited. As an inflammatory factor. IL-37 could show the pathological degree of nephridial tissue to a certain degree through its changes, which indicates that it might become the new target spot for the treatment of renal fibrosis. |
| keywords:IgA nephrosis IL-37 STAT3 |
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