白芍总苷改善维持性血液透析患者微炎症状态的临床研究

    Clinical Study of Total Glucosides of Paeony in Improving Micro-inflammation in Maintenance Hemodialysis Patients

    • 摘要: 目的 本研究旨在探讨白芍总苷(TGP)对维持性血液透析(MHD)患者微炎症状态的影响及其潜在机制。方法 收集60例MHD患者及30例体检正常者的临床资料,实验前、后抽取所有入组者的空腹静脉血,分别用生化仪检测血红蛋白(Hb)、白蛋白(Alb)、丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、超敏C反应蛋白(hs-CRP)水平,酶联免疫吸附法(Elisa)检测白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)和中性粒细胞明胶酶相关载脂蛋白(NGAL)水平,实时荧光定量聚合酶链反应(RT-PCR)检测Toll样受体4(TLR4)和髓样分化因子88(MyD88)水平。结果 MHD患者外周血hs-CRP、IL-6、TNF-α和NGAL的含量分别为(6.6±2.3)mg/L、(351.2±42.3)ng/L、(8.5±3.2)ng/L和(548.2±37.8)ng/ml,较正常对照组明显上升(P<0.05),差异具有统计学意义;给予TGP治疗后,上述指标分别为(4.2±2.3)mg/L、(298.5±52.7)ng/L、(7.3±3.3)ng/L和(440.6±42.0)ng/ml,较治疗前均明显下降(P<0.05),差异具有统计学意义。MHD患者外周血TLR4和MyD88 mRNA水平分别为(2.35±0.16)和(3.62±0.21),较正常对照组明显升高(P<0.05),差异具有统计学意义;给予TGP治疗后,上述指标分别为(1.28±0.14)和(1.64±0.24),较治疗前水平明显下降(P<0.05),差异具有统计学意义。结论 白芍总苷可能通过抑制TLR4/MyD88信号通路改善MHD患者微炎症状态,从而对MHD患者发挥保护作用。

       

      Abstract: Objective To investigate the effect of total glucosides of peony (TGP) on the micro-inflammation of patients with maintenance hemodialysis (MHD) and its underlying mechanism. Methods The clinical data of 60 patients with MHD and 30 healthy individuals were collected. The fasting venous blood was gathered before and after the experiment, and the content of hemoglobin (Hb), albumin (Alb), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and high-sensitivity C-reactive protein (CRP) was detrmined by biochemical analyzer. Enzyme-linked immunosorbent assay (Elisa) was employed to detect the levels of IL-6, TNF-α and neutrophil gelatinase-associated apolipoprotein (NGAL). Simultaneously, real-time fluorescence quantitative polymerase chain reaction (RT-PCR) was applied to examine Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88). Results As compared with the normal control group, the levels of CRP(6.6±2.3) vs. (1.2±1.4) mg/L, IL-6(351.2±42.3) vs. (55.3±8.4) ng/L, TNF-α(8.5±3.2) vs. (2.3±2.1) ng/L and NGAL(548.3±37.8) vs. (52.1±5.7) ng/mL in peripheral blood of MHD patients were significantly elevated (P<0.05). After treatment wiht TGP, the above indexes(4.2±2.3) vs. (6.8±2.7) mg/L,(298.5±52.7) ng/L vs. (349.2±50.2) ng/L,(7.3±3.3) vs. (8.8±3.1) ng/L and(440.6±42.0) vs.(549.92±42.84) ng/mL were significantly lower than those before treatment (P<0.05). The contents of TLR4(2.35±0.16)vs. (1.30±0.18) and MyD88 mRNA(3.62±0.21) vs. (1.58±0.15) in peripheral blood of MHD patients were remarkably higher than those in the normal control group (P<0.05). After the administration of TGP, the TLR4(1.28±0.14) vs. (2.42±0.24) and MYD88 concentration(1.64±0.24) vs. (3.68±0.19) was appreciably decreased as compared with those before treatment (P<0.05). Conclusions The TGP may improve the micro-inflammation of MHD patients by inhibiting the TLR4/MYD88/NF-κB signaling pathway, thus exerting protective effect on patients with MHD.

       

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