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目的探讨狼疮性肾炎(LN)肾脏细胞凋亡与细胞增殖的关系,加强LN发病机制的认识。方法用原位末端标记法(TUNEL)检测31例LN患儿及9例对照的肾组织细胞凋亡,用免疫组化及图像分析的方法检测PCNA(增殖细胞核抗原)及PDCD5、Caspase3的表达。结果(1)LN患儿肾组织中肾小球和肾小管的凋亡细胞、增殖细胞数、增殖细胞数/凋亡细胞数(P/A值)均明显高于对照组(LN组及对照组凋亡细胞、增殖细胞数、P/A值在肾小球分别为0.86±0.26比0.14±0.09,8.45±2.83比0.47±0.25,10.01±2.96比3.37±1.93,均P<0.01;在肾小管分别为1.16±0.42比0.16±0.07,13.73±3.54比1.32±0.15,12.81±3.91比8.94±1.79,均P<0.05)。(2)PDCD5在LN患儿肾小球的表达强度与对照组相比差异无统计学意义(0.09±0.05比0.08±0.02,P>0.05),在肾小管的表达强度明显低于对照组(0.13±0.05比0.21±0.07,P<0.01)。(3)Caspase3在LN患儿肾小球、肾小管的表达强度明显高于对照组(肾小球0.22±0.07比0.05±0.02,肾小管0.08±0.03比0.05±0.01,均P<0.01)。(4)直线相关分析显示:全部观察标本中肾小球凋亡细胞数与Caspase3的表达强度呈正相关(r=0.718,P<0.01),与PDCD5的表达强度无显著相关性(r=0.054,P>0.05);全部观察标本中肾小球、肾小管PDCD5的表达强度均与肾小球、肾小管Caspase3的表达强度无明显相关性(r=0.061,P>0.05,r=0.049,P>0.05)。多元逐步回归分析显示:在α=0.15水平上,全部观察标本中肾小管凋亡细胞数与PDCD5的表达强度呈负相关(回归系数为-3.686,t=-2.875,P=0.007),与Caspase3的表达强度呈正相关(回归系数为4.761,t=1.772,P=0.085)。结论(1)LN患儿肾组织细胞凋亡虽然比对照组增加,但相对细胞增殖来说表现为不足;(2)Caspase3参与了LN患儿肾组织肾小球、肾小管的细胞凋亡;(3)尚不能证实PDCD5参与了LN患儿肾小球细胞凋亡;但可能参与了肾小管的细胞凋亡。
Objective To investigate the relationship between cell apoptosis and cell proliferation in patients with lupus nephritis (LN) and to understand the pathogenesis of LN. Methods TUNEL was used to detect the apoptosis of renal tissue in 31 children with LN and 9 controls. The expression of PCNA (proliferating cell nuclear antigen), PDCD5 and Caspase3 were detected by immunohistochemistry and image analysis. Results (1) The number of apoptotic cells, the number of proliferating cells and the number of proliferating cells / apoptotic cells (P / A) in glomeruli and tubules of LN patients were significantly higher than those in control group (LN group and control group The number of apoptotic cells and proliferating cells in the glomerulus were 0.86 ± 0.26 vs 0.14 ± 0.09, 8.45 ± 2.83, 0.47 ± 0.25, 10.01 ± 2.96, 3.37 ± 1.93, respectively, P <0.01; Small tubes were 1.16 ± 0.42 vs 0.16 ± 0.07, 13.73 ± 3.54 vs 1.32 ± 0.15, 12.81 ± 3.91 vs 8.94 ± 1.79, all P <0.05). (2) The expression intensity of PDCD5 in glomeruli of LN patients was not significantly different from the control group (0.09 ± 0.05 vs 0.08 ± 0.02, P> 0.05), and the expression intensity of PDCD5 in renal tubules was significantly lower than that of the control group 0.13 ± 0.05 vs. 0.21 ± 0.07, P <0.01). (3) The expression of Caspase3 in glomeruli and tubules of LN patients was significantly higher than that in control group (glomerular 0.22 ± 0.07 vs 0.05 ± 0.02, tubular 0.08 ± 0.03 vs 0.05 ± 0.01, both P <0.01). (4) The linear correlation analysis showed that there was a positive correlation between the number of apoptotic glomeruli and the expression of Caspase3 (r = 0.718, P <0.01) in all the specimens and no significant correlation with the expression of PDCD5 (r = P> 0.05). The expressions of PDCD5 in glomeruli and tubules in all the specimens had no correlation with the expression of Caspase3 in glomeruli and tubules (r = 0.061, P> 0.05, r = 0.049, P> 0.05). Multivariate stepwise regression analysis showed that there was a negative correlation between the number of apoptotic tubular cells and the expression intensity of PDCD5 at the α = 0.15 level (regression coefficient = -3.686, t = -2.875, P = 0.007), and Caspase3 The expression intensity was positively correlated (regression coefficient was 4.761, t = 1.772, P = 0.085). Conclusions (1) Although the apoptosis of LN in children with LN is higher than that in the control group, the expression of Caspase3 is not enough in the proliferation of LN. (2) Caspase3 is involved in the apoptosis of glomerular and renal tubules in LN, (3) It has not been confirmed that PDCD5 is involved in glomerular apoptosis in LN patients, but it may be involved in renal tubular apoptosis.