高血压患者TLR4和胱抑素C的水平变化及作用

目的 探讨高血压患者外周血Toll受体4（Toll-like receptor 4,TLR4）、血清胱抑素C（Cystatin C,Cys-C）的表达水平及其作用和意义.方法 用流式细胞仪检测单纯高血压、高血压肾损害组患者及对照组外周血中单核细胞、中性粒细胞和淋巴细胞的TLR4表达率,并分析血清Cys-C、尿素氮（BUN）、血肌酐（SCr）、24 h尿蛋白等各项生化指标,比较各组间各项指标和水平的差异性及相关性.结果 高血压肾损害组的单核细胞及中性粒细胞表面TLR4表达率高于单纯高血压组[（54.71±10.57）]比（34.26±5.37）]（P〈0.01）,[（25.89±13.76）比（19.23±12.49）]（P〈0.05）;单纯高血压组单核细胞及中性粒细胞表面TLR4表达率高于对照组[（34.26±5.37）比（26.39±8.31）]（P〈0.01）;[（19.23±12.49）比（7.67±7.43）]（P〈0.01）,差异有统计学意义;3组淋巴细胞TLR4几乎无表达,无统计学差异（P〉0.05）.高血压肾损害组血清Cys-C均高于单纯高血压组（P〈0.01）,单纯高血压组显著高于对照组.单核细胞和中性粒细胞TLR4在高血压肾损害组的表达与Cys-C、SCr及24 h尿蛋白的值呈明显正相关;单纯高血压组单核细胞和中性粒细胞TLR4与Cys-C呈明显正相关,二者均与24 h尿蛋白和SCr无明显相关性（P〉0.05）.结论 TLR4在高血压和高血压肾损害患者的单核细胞和中性粒细胞中表达增高,同时Cys-C量升高,提示TLR4、Cys-C可能参与高血压的病理生理机制,介导高血压及靶器官损害.

Changes in toll-like receptor 4 and cystatin C in patients with hypertension and significance

Objective To explore the levels of toll-like receptor 4 in peripheral blood and serum cystatin C in patients with hypertension and the significance. Methods Flow cytometry was used to detect the positive expression rate of TLR4 in monocytes, neutrophil leucocytes and lymphocytes in peripheral blood in simple hypertensive group, hypertension plus renal damage group, and normal group. The TLR4, cystatin C, serum creatinine and 24 h urinary total protein were analyzed. Results The positive expression rate of TLR4 in monocytes and neutrophil leucocytes in hypertension plus renal damage group was higher than in simple hypertensive group （54. 71 ± 10. 57 vs 34. 26 ± 5.37,P 〈0. 01 ; 25.89 ± 13. 76 vs 19. 23 ± 12. 49,P〈0. 05）, and that in simple hypertensive group was higher than in normal group （34. 26 ± 5.37 vs 26. 39 ± 8.31, P〈0. 01 ; 19. 23 ± 12. 49 vs. 7. 67 ± 7. 43, P〈 0. 01）. The positive expression rate of TLR4 in lymph ocytes was low and showed no significant difference among the three groups （P〈0. 05）. Serum cystatin C level was higher in hypertension plus renal damage group than in simple hypertensive group, and that in simple hypertensive group was higher than in normal group. The TLR4 expression in hypertension plus renal damage group showed a significantly positive correlation with Cys-C, SCr and UTP/24 h in monocytes and neutrophil leucocytes, but that in simple hypertensive group showed a positive correlation with cystatin C in monocytes and neutrophil leucocytes. In simple hypertensive group and hypertension plus renal damage group,TLR4 and Cys-C showed no significant correlation with SCr and UTP/24 h （P〉0. 05） in monocytes and neutrophil leucocytes. Conclusions The expression of TLR4 is elevated in monocytes and neutrophil leucocytes, so did cystatin C. We hypothesize TLR4 and Cys-C may be involved in the pathological mechanism and development of hypertension and mediate target organ damage.