Objective To explore the correlation between stagnated heat syndrome and clotting

inflammation in hemorrhagic stroke patients. Methods Hemorrhagic stroke patients with stagnated heat syndrome and non-stagnated heat syndrome were selected and divided into stagnated heat group and non-stagnated heat group

with 9 patients in each group. The blood samples of both groups were collected to extract lymphocytes. High-throughput sequencing was applied to detect gene expressions. The functions and pathways of the differentially expressed genes were analyzed.Results There was significant difference in gene expression spectrum of both groups. Compared with the non-stasis heat group

there were 2867 genes whose expression was up-regulated ≥2 times

and 1877 genes whose expression was down-regulated ≥2 times. The pathways that related to differentially expressed genes were coagulation-related pathways

inflammatory immune-related pathways

vascular endothelial pathways

apoptosis

and cell cycle related pathways. Real-time PCR was used to verify the expression of tumor necrosis factor receptor superfamily 18（ TNFRSF18）

matrix metalloproteinase 23 B（ MMP23 B）

DNAJ homologous B subfamily 14（ DNAJB14）

interleukin 2 receptor α（ IL2 RA）

C1 Q tumor necrosis factor 3（ C1 QTNF3）

pleteletdericed growth factor（ PDGFRB）

blood coagulation factor Ⅷ（ F8） and blood coagulation factor Ⅱ（ F2）

and the results were consistent with the gene chip. Conclusion The essential feature of hemorrhagic stroke of stagnated heat syndrome is related to clotting and inflammation. Stasis elicited by stagnation of blood and heat caused by inflammatory reaction might be the nature of hemorrhagic stroke with stagnated heat syndrome.