OBJECTIVE:To explore the novel biomarkers and therapeutic target candidates related to the stasis-heat syndrome of acute intracerebral hemorrhage(AICH).METHODS:Applying an isobaric tagging for relative and absolute qu...OBJECTIVE:To explore the novel biomarkers and therapeutic target candidates related to the stasis-heat syndrome of acute intracerebral hemorrhage(AICH).METHODS:Applying an isobaric tagging for relative and absolute quantitation-(i TRAQ-)based quantitative proteomic approach,plasma samples from AICH patients with stasis-heat,and AICH patients with non-stasis-heat and healthy control subjects were collected and analyzed to distinguish differentially expressed proteins(DEPs)correlated to AICH with stasis-heat in this block design.The standard Western blot was applied to verify DEPs.Additionally,DEPs were analyzed via bioinformatic platforms and further approved via Ingenuity Pathway Analysis(IPA).RESULTS:A total of 26 DEPs were found among AICH with the stasis-heat,AICH with non-stasis-heat,and healthy control group.The seven DEPs compared with the non-stasis-heat group are closely related to the pathogenesis of stasis heat.These proteins showed three different protein expression patterns.The alpha-1-b glycoprotein(A1 BG)and copper-protein(CP)were upregulated in the stasis-heat group,but down-regulated in the non-stasis-heat group.Compared with the non-stasisheat group,the expression abundance of actinin,alpha 1(ACTN1),carbonic anhydrase I(CA1),peroxiredoxin 2(PRDX2),and vinculin(VCL)is higher in the stasis-heat group,while the CD44 is the opposite.These differences reflect that stasis-heat syndrome has more severe inflammatory immune response,coagulation disorders and damage.Bioinformatics analysis revealed that a wide variety of cellular and metabolic processes and some signaling pathways were involved in the pathophysiology of AICH with stasis-heat.AICH with stasis-heat syndrome showed more severe inflammatory reactions,tissue damage,and coagulation disorders than non-stasis heat syndrome.CONCLUSIONS:There are differences in the protein expression patterns between the stasis-heat syndrome and non-stasis-heat syndrome.These differences reflect that stasis-heat syndrome has more severe damage.CD44,CP,ACTN1,CA1,VCL,展开更多
基金Supported by Jiangsu Province Social Development Key Research and Development Program:Construction and Application of Decision Support System of TCM Master Zhou Zhongying’s Experience Learning in Distinguishing and Treating Major Diseases based on the Intelligent Technology(No.BE2019723)the National Natural Science Foundation of China:Dynamic Measurement and Study of Biomarker on Pathogenic Unit of Stasis-Heat in Acute Intracerebral Hemorrhage(No.813735)
文摘OBJECTIVE:To explore the novel biomarkers and therapeutic target candidates related to the stasis-heat syndrome of acute intracerebral hemorrhage(AICH).METHODS:Applying an isobaric tagging for relative and absolute quantitation-(i TRAQ-)based quantitative proteomic approach,plasma samples from AICH patients with stasis-heat,and AICH patients with non-stasis-heat and healthy control subjects were collected and analyzed to distinguish differentially expressed proteins(DEPs)correlated to AICH with stasis-heat in this block design.The standard Western blot was applied to verify DEPs.Additionally,DEPs were analyzed via bioinformatic platforms and further approved via Ingenuity Pathway Analysis(IPA).RESULTS:A total of 26 DEPs were found among AICH with the stasis-heat,AICH with non-stasis-heat,and healthy control group.The seven DEPs compared with the non-stasis-heat group are closely related to the pathogenesis of stasis heat.These proteins showed three different protein expression patterns.The alpha-1-b glycoprotein(A1 BG)and copper-protein(CP)were upregulated in the stasis-heat group,but down-regulated in the non-stasis-heat group.Compared with the non-stasisheat group,the expression abundance of actinin,alpha 1(ACTN1),carbonic anhydrase I(CA1),peroxiredoxin 2(PRDX2),and vinculin(VCL)is higher in the stasis-heat group,while the CD44 is the opposite.These differences reflect that stasis-heat syndrome has more severe inflammatory immune response,coagulation disorders and damage.Bioinformatics analysis revealed that a wide variety of cellular and metabolic processes and some signaling pathways were involved in the pathophysiology of AICH with stasis-heat.AICH with stasis-heat syndrome showed more severe inflammatory reactions,tissue damage,and coagulation disorders than non-stasis heat syndrome.CONCLUSIONS:There are differences in the protein expression patterns between the stasis-heat syndrome and non-stasis-heat syndrome.These differences reflect that stasis-heat syndrome has more severe damage.CD44,CP,ACTN1,CA1,VCL,
