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目的:探讨巨噬细胞特异表达共刺激分子VSIG4与实验性小鼠肾间质纤维化的关系。方法:SPF级雄性C57B6(VSIG4-/-及VSIG4+/+)小鼠共40只,其中VSIG4-/-肾小管间质性肾炎模型组(n=20)和VSIG4+/+肾小管间质性肾炎模型组(n=20),两个模型组下分别设术前7d及单侧输尿管梗阻后3d、7d、14d4个时相点,每个时相点各5只。模型组行左输尿管结扎。采用自动生化分析仪检测小鼠血肌酐、尿素氮水平。于术前7d、术后第3、7、14天观察肾小管损害及肾间质炎性细胞浸润程度,免疫组化技术观察病变肾组织TGF-β1和MMP-2的表达。结果:①血肌酐及尿素氮水平在两个模型组间无统计学意义。②与VSIG4+/+肾小管间质性肾炎模型组相比,VSIG4-/-肾小管间质性肾炎模型组肾间质炎性细胞浸润和肾小管损害程度明显加重(P<0.05),肾组织TGF-β1表达明显升高(P<0.05),MMP-2表达显著降低(P<0.01)。结论:VSIG4-/-的小鼠肾间质炎性细胞浸润、肾小管损害加重,病变肾组织TGF-β1的表达上升和MMP-2的表达下调。提示VSIG4在抑制肾小管间质损伤的病理进程中发挥作用。
Objective: To investigate the relationship between macrophage-specific costimulatory molecule VSIG4 and experimental mouse renal interstitial fibrosis. Methods: A total of 40 SPF male C57B6 (VSIG4 - / - and VSIG4 + / +) mice, including VSIG4 - / - tubulointerstitial nephritis model group (n = 20) and VSIG4 + / + tubulointerstitial nephritis Model group (n = 20). The two models were divided into 4 time points at pre-operative 7d and unilateral ureteral obstruction at 3d, 7d and 14d, and 5 at each time point. Model group left ureteral ligation. Serum creatinine and urea nitrogen levels were measured by automatic biochemical analyzer. The degree of renal tubule damage and interstitial infiltration of inflammatory cells were observed on the 7th day before operation and on the 3rd, 7th and 14th day after operation. The expressions of TGF-β1 and MMP-2 in the diseased kidneys were observed by immunohistochemistry. Results: ① Serum creatinine and urea nitrogen levels were not statistically significant between the two model groups. ②Compared with VSIG4 + / + tubulointerstitial nephritis model group, interstitial inflammatory cell infiltration and tubular damage were significantly increased in VSIG4 - / - tubulointerstitial nephritis model group (P <0.05), renal tissue TGF-β1 expression was significantly increased (P <0.05), MMP-2 expression was significantly lower (P <0.01). CONCLUSION: The interstitial infiltration of renal interstitium and the damage of renal tubules in VSIG4 - / - mice increased, while the expression of TGF-β1 and the expression of MMP-2 in renal tissues decreased. Tip VSIG4 in tubulointerstitial damage in the pathological process play a role.