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目的观察结缔组织生长凶子(CTGF)在慢性移植物抗宿主病(cGVHD)狼疮样小鼠。肾组织中的表达情况及氟伐他汀的调节作用。方法建立cGVHD狼疮样小鼠模型。按随机设计原则将模型小鼠分为3组,即模型对照组(A组)、氟伐他汀干预组(B组)及正常对照组(C组),每组均有6只小鼠。CTGF蛋白检测采用免疫组织化学方法及免疫荧光法．mRNA表达采用反转录-聚合酶链反应(RT-PCR)检测：留取24 h尿,测定尿蛋白排泄量。结果模型对照组小鼠24 h尿蛋门总量明显高于氟伐他汀干预组(P＜0．05)及正常对照组小鼠(P＜0．01)；RT-PCR检测到模型对照组小鼠肾组织CTGF mRNA表达较氟伐他汀干预组小鼠明显升高(P＜0．05),而正常对照组小鼠表达量少；免疫组织化学及免疫荧光表明正常对照组小鼠仅在少数肾小管有微量CTGF表达,而模型对照组及氟伐他汀干预组小鼠肾小管及问质均有CTGF蛋白表达,且模型对照组小鼠表达量显著高于氟伐他汀干预组小鼠(P＜0．01)。结论CTGF可能参与介导狼疮肾炎的发生、发展；cGVHD狼疮样小鼠模型肾组织中CTGF蛋白及mRNA表达明显上调,提示CTGF可能在狼疮肾炎(LN)肾小球硬化及肾间质纤维化的进程中起重要作用；氟伐他汀可能通过降低CTGF表达及减少尿蛋白排泄从而缓解LN,延缓肾纤维化进程。
Objective To observe the growth of connective tissue fusants (CTGF) in chronic graft-versus-host-disease (cGVHD) lupus-like mice. Renal Tissue Expression and Fluvastatin Regulatory Function. Methods The cGVHD lupus-like mouse model was established. According to the principle of random design, the model mice were divided into three groups: model control group (A group), fluvastatin intervention group (B group) and normal control group (C group), each group had 6 mice. CTGF protein detection using immunohistochemistry and immunofluorescence. mRNA expression was detected by reverse transcription-polymerase chain reaction (RT-PCR): 24 h urinary retention, urinary protein excretion was measured. Results The total amount of urinary door in 24 h urine in the model control group was significantly higher than that in fluvastatin intervention group and normal control group (P <0.01). RT-PCR results showed that the model control group The expression of CTGF mRNA in the kidney of mice was significantly higher than that of the mice treated with fluvastatin (P <0.05), while the expression of CTGF mRNA in the normal control group was less than that of the mice treated with fluvastatin. Immunohistochemistry and immunofluorescence showed that the mice in normal control group A small number of renal tubules with a small amount of CTGF expression, while the model control group and fluvastatin intervention group tubulointerstitial and CTGF protein expression, and the model control group was significantly higher expression of mice than fluvastatin intervention group mice ( P <0.01). Conclusion CTGF may be involved in the pathogenesis and development of lupus nephritis. The expression of CTGF protein and mRNA in cGVHD lupus-like mouse model was significantly up-regulated, suggesting that CTGF might be associated with glomerulosclerosis and renal interstitial fibrosis in lupus nephritis (LN) Plays an important role in the process; fluvastatin may delay the process of renal fibrosis by reducing CTGF expression and reducing urinary protein excretion to relieve LN.