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目的 探讨霉酚酸在体外对小鼠肾小球系膜细胞增殖及其分泌单核细胞趋化因子1的影响。方法 在小鼠肾小球系膜细胞的培养基中加入不同浓度的霉酚酸(0.1、1、5 及10μmol/L),培养24 h,采用四甲基偶氮唑盐掺入法,以酶联免疫检测仪测定各组570 nm波长的吸光度值,以计算肾小球系膜细胞的存活率;另在肾小球系膜细胞的培养基中加入不同浓度的霉酚酸(0、0.5及2.5μmol/L),并同时加入肿瘤坏死因子(20 ng/ml)、白细胞介素1β(2 ng/ml)及γ干扰素(10 ng/ml)刺激4 h,收集上清液,测定单核细胞趋化因子1浓度,并行淋巴细胞迁移实验。结果 培养基中加入霉酚酸者,肾小球系膜细胞的增殖受到明显的抑制,并呈剂量依赖性;在肿瘤坏死因子、白细胞介素1β及γ干扰素的刺激下,培养的肾小球系膜细胞分泌单核细胞趋化因子1 明显增加,加入霉酚酸后,能明显抑制单核细胞趋化因子1的分泌(P<0.01),并能抑制淋巴细胞的迁移。结论 霉酚酸在体外可以抑制肾小球系膜细胞的增殖及趋化性细胞因子的分泌,这为临床上研究慢性移植肾肾病的发生和发展提供实验依据。
Objective To investigate the effects of mycophenolic acid on the proliferation of rat mesangial cells and the secretion of monocyte chemoattractant 1 in vitro. Methods Different concentrations of mycophenolic acid (0.1, 1, 5 and 10 μmol / L) were added to the culture medium of mouse glomerular mesangial cells and cultured for 24 h. Tetramethylzirconate The absorbance of 570 nm wavelength in each group was measured by enzyme-linked immunosorbent assay to calculate the survival rate of glomerular mesangial cells. Different mycophenolic acid (0, 0.5) was added to the culture medium of glomerular mesangial cells And 2.5μmol / L, respectively). The supernatants were also stimulated with tumor necrosis factor (20 ng / ml), interleukin 1β (2 ng / ml) and interferon gamma (10 ng / Monocyte Chemokine 1 Concentration, Parallel Lymphocyte Migration Assay. Results When mycophenolic acid was added to the culture medium, the proliferation of glomerular mesangial cells was significantly inhibited and in a dose-dependent manner. Under the stimulation of tumor necrosis factor, interleukin-1β and interferon-γ, The mesangial cells secreted monocyte chemotactic factor 1 increased significantly, after adding mycophenolic acid, can significantly inhibit the secretion of monocyte chemotactic factor 1 (P <0.01), and can inhibit the migration of lymphocytes. Conclusion Mycophenolic acid can inhibit the proliferation of mesangial cells and the secretion of chemokines in vitro, which provides experimental evidence for the study of the occurrence and development of chronic allograft nephropathy in clinic.