RESUMO
The therapeutic effect of Uighur prescription on abnormal Savda in asthma patients was evaluated using plasma proteomics in order to elucidate the biological mechanism and identify potential therapeutic targets of abnormal Savda. In the present study, 40 asthma patients with abnormal Savda including abnormal Savda Munziq and Savda Mushil were enrolled and treated with Uighur prescription. The effect of Uighur prescription on protein expression and potential targets was investigated by isobaric tags for relative and absolute quantitation (iTRAQ)-based proteomics and bioinformatics analysis. Expression of candidate proteins was verified by an enzyme-linked immunosorbent assay. Following treatment with the Uighur prescription, 22 proteins were differentially expressed in the plasma of patients with asthma and abnormal Savda. The majority of these proteins were localized in intermediate filaments and the cytoskeleton and acted as antioxidant enzymes and binding proteins. Furthermore, they participated in the defense and inflammatory response, and the response to oxidative stress and wound healing. Peroxiredoxin 2 and carboxypeptidase B2 expression was significantly upregulated, whereas S100A7 was considerably downregulated in the whole plasma of patients (all P<0.05) in accordance with the iTRAQ proteomics data. Uighur prescription of abnormal Savda may affect the whole regulatory network of protein expression that is altered following the development of abnormal Savda in patients with asthma.
RESUMO
BACKGROUND: Increased levels of interleukin-6 (IL-6) and C-reactive protein (CRP) have been reported in patients with venous thromboembolisms (VTE). However, prospective studies did not confirm an association between IL-6, CRP and their polymorphism with the risk of VTE. METHODS: One hundred and forty patients (including 66 males and 74 females, mean age (55.55 ± 17.11) years) and one hundred and sixty controls (including 74 males and 86 females, mean age (56.58 ± 12.24) years) were involved. An enzyme linked immunosorbent assay (ELISA) method was used for detecting the serum levels of inflammatory factors IL-6 and CRP in both groups. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used for analyzing the distribution of polymorphisms at the -572C/G and -597G/A sites of the promoter of the IL-6 gene and at 1059G/C of the CRP gene. RESULTS: Serum levels of IL-6 and CRP were significantly higher in the VTE group than in the control group (P < 0.05). The frequencies of -572C/G promoter polymorphisms CC, CG, and GG in the IL-6 gene were found to be 34%, 48%, and 18%, respectively, and the derived allele frequencies for the C and G alleles were 58% and 42%. There was a significant difference in the -572C/G promoter polymorphisms between the VTE group and control group (P < 0.05). For the -597G/A polymorphism, individuals all carried the GG and GA type; AA genotypes were not detected. The frequency of the GG, GC, and CC genotypes at the CRP1059G/C promoter was 87.57%, 7.86% and 3.57% in VTE group, while 86.25%, 10%, and 3.75% in control group, respectively. The frequency of G and C alleles at CRP 1059G/C was 91.43% and 8.57% in VTE group and 91.56% and 8.44% in the control group. The results showed that there was no statistically significant difference of 1059G/C genotype and mutation frequency of the allele between the VTE group and control group (P > 0.05). Multiple Logistic regression analysis showed CC homozygotes of the IL-6 -572G/C, body mass index (BMI), and CRP, IL-6, and high-density lipoprotein cholesterol (HDL-C) were independent risk factors for VTE (P < 0.05). CONCLUSIONS: We found that VTE was associated with IL-6 and CRP levels, and there was an association of IL-6 and its promoter polymorphism at -572G/C with the risk of VTE. Thus far, a causal relationship between inflammation and VTE remains to be clarified and more prospective data are required.
