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Objective To explore the expert survey of the weight and the current common weight of the similarities and differences in the quantitative analysis of the symptoms in syndrome evaluation. Methods Through the expert questionnaire survey, the data of the questionnaire were analyzed by SPSS11.5 software. For the question of whether the weight of each symptom was the same, the frequency of the experts who gave yes and no was calculated. For the weight of the specific number of such openness, the weight given by the experts was listed firstly, and then the weight of frequency of each expert was calculated, and the frequency of the largest weight was selected as the weight of the symptoms to determine the weight of the syndrome quantification assignment in the evaluation of the efficacy of the syndrome, and to compare the obtained weight with the current weight. Results The weight of the two methods is very close in the weight of the primary symptom and the weight of secondary symptom. But as for whether the weight of the primary symptom and secondary symptom is the same, the majority of the experts think that it should be different, and the current usual practice is to give the same weight. Conclusion During the weight determination, not every primary symptom or secondary symptom is the same important. Therefore, the practice of giving the same weight to evry primary symptom and secondary symptom is questionable.
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Aim To investigate the effects and mechanisms of CCK-8 on IL-1? induced proliferation of RSC-364, a rat fibroblast-like synovial cell line. Methods MTT colorimetric assay and Western blot were used to measure cell proliferation and p38MAPK phosphorylation level to elucidate the mechanism of CCK-8 in IL-1? induced RSC-364 proliferation. Results CCK-8 significantly inhibited IL-1?-induced RSC-364 proliferation at 10 -12 , 10 -10 , 10 -8 , 10 -6 mol ? L -1 , and IL-1?-activated p38MAPK activity at 10 -10 , 10 -8 , 10 -6 mol?L -1 in a dose-dependent manner. The effect of CCK-8 was blocked by CR1409 (a CCKA-receptor antagonist) and CR2945 (a CCKB-receptor antagonist). Conclusion CCK-8 inhibits IL-1?-induced RSC-364 proliferation, probably by reducing p38MAPK activity through CCKA and CCKB receptors.
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Aim To investigate the effects of cholecystokinin-octopeptide on IL-12 secreted in murine bone marrow-derived dendritic cells induced by lipopolysaccharide.Methods The CCK receptor subtypes were investigated by immunofluorescence in murine bone marrow-derived dendritic cells.Enzyme linked immunosorbent assay and Western blot were used to estimate the contents of IL-12 and p38MAPK activity.Results CCK-1R and CCK-2R were detected in BM-DC;CCK-8(at concentrations of 10-10,10-8,10-6 mol?L-1)could significantly increase the secretion of IL-12 in the LPS-induced DC, and LPS-activated p38MAPK activity in a dose-dependent manner.The effect of CCK-8 was reduced partially by CR1409(a CCK-1R antagonist) and CR2945(a CCK-2R antagonist).Conclusion CCK-8 could dose-dependently increase the expressions of IL-12 in LPS-induced DC,probably by promoting p38MAPK activity and the effect was mediated by CCK1 and CCK2 receptors.