Proteomic Study Of Human Serum In The “Congenital Fu-han”(CFH) Syndrome

PurposeIn this study, serums from patients with the “congenital Fu-Han”(CFH) syndrome, the kidney Yang-deficiency syndrome, healthy subjects, and patients after interventions of the CFH syndrome are investigated via comparative proteomic analysis. Using bioinformatics and statistical methods on the differentially expressed proteins, relationships between proteins and the two syndromes are unveiled. Through establishment of protein expression profiles of the CFH syndrome and identification of key proteins via mass spectrometry, potential roles of these proteins as markers of the CFH syndrome are proposed. Method:The experiments are designed on the basis of the combination of disease and syndrome. Two-dimensional gel electrophoresis and biological mass spectrometry techniques are used for isolation and identification of differentially expressed proteins between each of the syndrome groups and the healthy group, as well as the ones between the pre- and postintervention groups of the CFH syndrome. Statistical analysis of the differentially expressed proteins is used to find the underlying molecular substances of the CFH syndrome as a suboptimal health status, which builds the material basis of this syndrome from a view of molecular biology. Result1. In comparison with the healthy group, 28 differentially expressed protein spots are detected in the CFH group, with 9 upregulated and 19 downregulated; 28 protein spots are detected in the kidney Yang-deficiency group as well, with 15 upregulated and 13 downregulated. Meanwhile, 36 protein spots are detected in the CFH group compared with the kidney Yang-deficiency group, with 20 upregulated and 16 downregulated.2. Among the differentially expressed proteins in the CFH group compared with the healthy group, complement C4 and keratin are upregulated, while complement factor H, complement C6, complement factor I, biliverdin Su reductase, vitamin D binding protein, heme-binding protein, plasma serine protease inhibitor, human chorionic gonadotropin and kininogen are downregulated. After the drug intervention, the CFH group shows a decrease in the expression levels of complement C4 and keratin, while an increase of Biliverdin reductase, heme binding protein and vitamin D binding protein.3. It is also observed that compared with the healthy group, the kidney Yang-deficiency group shows upregulation of glycoproteins, biliverdin reductase, vitamin D binding protein, protein clusters, keratin, catalase inhibitor and carbonic anhydrase, while downregulation of complement factor C4, blood fibronectin and carboxypeptidase catalyst.4. Comparative analysis of the differentially expressed proteins reveals the similarities and differences between the two syndrome groups. Compared with the healthy group, both groups show upregulation of keratin and downregulation of heme-binding proteins. While the biliverdin reductase and vitamin D binding protein are downregulated in the CFH group, they are upregulated in the kidney Yang-deficiency group. Complement C4 expression is upregulated in the CFH group, while in the kidney Yang-deficiency group it is downregulated. ConclusionSignificant differences of proteomic profiles between either syndrome group and the healthy group are detected, suggesting that both syndromes are in suboptimal health status. Nevertheless, significant differences between the kidney Yang-deficiency group and the CFH group also reveal the differences between the two syndromes. While the kidney Yang-deficiency group shows abnormal expressions of glycoprotein, the CFH group have more abnormalities of the complement system. In addition, interventions of the CFH group witnesses the adjustment of the expression levels of proteins related the body’s immune system and arteriosclerosis, suggesting that early identification and intervention is of great significance to the prevention of disease.