BACKGROUND: There are some cytokines like interleukin-6, tumor necrosis factor-alpha as well as neurohormones such as norepinerphrine in serum of patients with congestive heart failure. However, whether they influence the occurrence and development of congestive heart failure is uncertain.OBJECTIVE: To explore the changes and significance of interleukin-6,tumor necrosis factor-alpha and norepinerphrine in order to provide basis for assessing the severity of heart failure and its prognosis.DESIGN: A case control study.SETTING: Department of Cardiology, Shidong Hospital of Shanghai City.INTERVENTIONS: A total of 58 patients with congestive heart failure admitted to Department of Cardiology, Shidong Hospital of Shanghai City from January 2000 to October 2001 were chosen as patient group with 33 males and 25 females. According to NYHA heart function classification,there were 12 cases of level Ⅱ, 32 cases with level Ⅲ and 14 cases of level Ⅳ. Thirty healthy volunteers who took physical examination during the same time were chosen as control group with 18 males and 12 females.ELISA was used to assay the levels of interleukin-6, tumor necrosis factoralpha and norepinerphrine in serum while two-dimension echocardiography was used to test the left ventricular ejection fraction in order to observe the relationship between cytokines and heart function.RESULTS: ① The levels of interleukin-6 [(367.6±78.6), (569.7±117.3)ng/L], tumor necrosis factor-alpha [(395.3±82.4), (583.1±124.8) ng/L] and norepinerphrine [(396.5±85.3),(675.9±136.2) ng/L] in patients with level Ⅰ-Ⅱ, Ⅳ heart function was remarkably higher than those of patients with level Ⅱ heart function and people in control group[(221.5±58.4), (170.2±42.7)ng/L; (205.4±59.2), (180.3±43.8) ng/L; (227.4±65.6),(163.8±41.5) ng/L] (P ＜ 0.05). Compared patients of level Ⅱ heart function with people in the control group, there was no difference on the above indicators (P ＞ 0.05).②There was highly negative correlation between interleukin-6, tumor necrosis factor-alpha, norepinerphrine and left ventricular ejection fraction (r=-0.63, P＜ 0.01; r=-0.54, P＜ 0.05;r=-0.58,P ＜ 0.01). The more severe the heart failure, the higher the levels of interleukin-6, tumor necrosis factor-alpha and norepinerphrine. There was obviously positive correlation between tumor necrosis factor-alpha and norepinerphrine as well as between interleukin-6 and norepinerphrine (r=0.57,P ＜ 0.01;r=0.51,P ＜ 0.05). The more severe the heart failure, the higher the level of interleukin-6 and tumor necrosis factor-alpha and that there was positive correlation between them (r=0.39, P ＜ 0.05).CONCLUSION: The tumor necrosis factor-alpha and interleukin-6 levels in patients with congestive heart failure all increased, especially in patients with moderate or severe congestive heart failure, and represented negative correlation with left ventricular ejection fraction. It suggests that the levels of interleukin-6, tumor necrosis factor-alpha in serum can be used as indicators to assess the severity and prognosis of congestive heart failure and provide assessment basis for quantitative evaluation of rehabilitation interventions.

ObjectiveTo explore the compatibility advantage of Scutellariae Radix-Coptidis Rhizoma in the prevention and treatment of neuroinflammation， and to elucidate the action characteristics and mechanism of the compatibility advantage based on Toll like receptor （TLR4）/myeloid differentiation factor 88 （MyD88）/nuclear factor kappaB （NF-κB） pathway. MethodRepresentative mouse microglia cells （BV2） in vitro were selected and divided into 8 groups： control group， model group， Scutellariae Radix-Coptidis Rhizoma group， Piracetam group， Scutellariae Radix group and Coptidis Rhizoma group. The BV2 cell inflammatory model was established by lipopolysaccharide （LPS）， and the cell activity was detected by cell counting kit-8 （CCK-8）. Cell morphology was observed under bright field. The production and release of pro-inflammatory factors in BV2 cells were determined by enzyme-linked immunosorbent assay （ELISA） and immunofluorescence assay， and the mRNA expressions of TLR4， MyD88 and NF-κB were detected by Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. The nuclear translocation of NF-κB p65 was detected by immunofluorescence， and TLR4 signal transduction inhibitor （CLI-095） and NF-κB inhibitor （PDTC） were used to confirm the anti-neuroinflammation targets of Scutellariae Radix-Coptidis Rhizoma. ResultCompared with the conditions in the control group， most cells in LPS-induced model group were activated， and the contents of IL-6， TNF-α and IL-1β in culture medium and cells and the mRNA expressions of TLR4， MyD88， NF-κB p50 and NF-κB p65 were increased （P<0.01）， with obvious nuclear entry of NF-κB p65. Compared with the conditions in the model group， BV2 cell morphology was mostly recovered after pretreatment in Scutellariae Radix-Coptidis Rhizoma and Piracetam groups， and the levels of IL-6， TNF-α and IL-1β and the mRNA expressions of TLR4， MyD88， NF-κB p50 and NF-κB p65 were decreased （P<0.05， P<0.01）， with NF-κB p65 mostly observed in cytoplasm. Compared with the conditions in the model group， cell morphology was slightly recovered in Scutellariae Radix group and Coptidis Rhizoma group， and the levels of pro-inflammatory factors and mRNA expressions of TLR4， MyD88， NF-κB p50 and NF-κB p65 were reduced. In terms of inhibitory effect on pro-inflammatory factors， Scutellariae Radix group and Coptidis Rhizoma group were lower than Scutellariae Radix-Coptidis Rhizoma group （P<0.05）. Compared with the model group， the "Scutellariae Radix-Coptidis Rhizoma+CLI-095" group and "Scutellariae Radix-Coptidis Rhizoma+PDTC" group had lowered mRNA expressions of TLR4， MyD88， NF-κB p50 and NF-κB p65 （P<0.05， P<0.01）， and the transfer of NF-κB p65 into nucleus was obviously inhibited. ConclusionThe anti-neuroinflammation effect of Scutellariae Radix-Coptidis Rhizoma was significantly better than Scutellariae Radix or Coptidis Rhizom alone， and the anti-neuroinflammation advantage was closely related to the inhibition of activation of TLR4/MyD88/NF-κB signaling pathway in microglial cells. It was confirmed that TLR4， MyD88 and NF-κB were potential targets for Scutellariae Radix-Coptidis Rhizoma to exert the compatibility advantage.