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目的研究霉酚酸脂(mycophenolate mofetil,MMF)对免疫复合物所致肾脏损伤的保护作用及机制。方法30只清洁级SD大鼠,雌雄各半,随机分为3组,每组10只。采用阳离子化牛血清白蛋白(C-BSA)建立免疫复合物型大鼠肾炎模型。从预免疫开始,给予MMF 60 mg/(kg·d),连续给药8周,实验期间,观察大鼠的体重、精神状况,24 h尿蛋白测定。实验结束麻醉采血进行生化血液学检测,保留肾脏组织进行组织病理学检查,采用免疫组化方法检测肾脏组织中Ig G、C3的沉积。结果 MMF组大鼠从第4周起平均体重轻于相应时间的正常对照组大鼠平均体重(P<0.01或P<0.05),但体重减轻的程度比模型组有所降低。MMF组各个时间点的尿蛋白水平虽比正常对照组增加,但与模型组相比均显著降低(P<0.01)。与模型组比较,MMF组能显著降低CHO和BUN,升高Alb(P<0.05)。病理学检查发现MMF组可改善肾小球与肾小管的病理损伤。免疫荧光半定量分析可见模型组肾脏的Ig G、C3沉积显著高于MMF组。结论 MMF能减轻免疫复合物所致的肾脏损伤,可能与其能抑制肾脏系膜细胞及系膜基质增生有关,其机制还有待进一步研究。
Objective To investigate the protective effect and mechanism of mycophenolate mofetil (MMF) on immune injury caused by immune complex. Methods Thirty clean-grade SD rats were randomly divided into 3 groups with 10 mice in each group. Immunocomplex-induced rat nephritis model was established by cationized bovine serum albumin (C-BSA). From pre-immunization, given MMF 60 mg / (kg · d), continuous administration of 8 weeks, during the experiment to observe the body weight, mental status, 24 h urinary protein determination. At the end of the experiment, blood was collected for biochemical hematology test, histopathological examination was performed on the kidney and the deposition of Ig G and C3 in the kidney was detected by immunohistochemistry. Results The average weight of rats in MMF group was lighter than that of normal control rats from the fourth week (P <0.01 or P <0.05), but the degree of weight loss was lower than that of the model group. Urinary protein levels in MMF group at various time points were higher than those in normal control group, but were significantly lower than those in model group (P <0.01). Compared with model group, MMF group could significantly decrease CHO and BUN and increase Alb (P <0.05). Pathological examination found that MMF group can improve the glomerular and tubular pathological injury. Immunofluorescence semi-quantitative analysis of the model group showed Ig G, C3 deposition was significantly higher than the MMF group. CONCLUSION: MMF can reduce the renal damage induced by immune complex, which may be related to the inhibition of mesangial cells and mesangial matrix proliferation. The mechanism needs to be further studied.