The Relationship Between The CD163/HO-1Pathway And Inflammation In Perihematoma Tissue Atfer Human Cerebral Hemorrhage

Intracerebral hemorrhage accounted for15%-20%of all type of stroke and themortality and invalid rate are higher than other subtypes. at present, thepathogenesis is not entirely clear.CD163/HO-1pathway was thought to the mainmetabolic pathway of hemoglobin and may have a potential antiinflammatory andantioxidant role. Thus, we established this experiment to study the dynamicexpression of CD163and HO-1in around the hematoma tissue after intracerebralhemorrhage, and detect the relationship between their expression and theinflammatory response. In this study, we selected27patients with hypertensivecerebral hemorrhage who were all under craniotomy and hematoma removal, andtook brain tissue from about1cm near to the hematoma as a experimental group andbrain tissue away from the hematoma as controls during the approach.All Specimenswere divided into three sub-groups:≤6h group,6~24h group,24~72h group and>72h group according to the time interval between onset to taking samples. HE staining,TUNEL staining and immunohistochemical method were used to observe thepathological changes, apoptosis and detect the expression of TNF-α, IL-1and IL-10.RT-PCR, western blot and immunohistochemical methods respectively, were used todetect the expression of CD163on gene and protein levels, and analysed correlationof CD163with TNF-α, IL-1and IL-10expression. RT-PCR, western blot andimmunohistochemical methods respectively, were used to detect the expression ofHO-1on gene and protein levels, and analysed correlation of HO-1with TNF-α andIL-1expression. Correlation between CD163and HO-1expression was analysed.We found Significant difference between experimental group and control group fromHE stain. TUNEL-positive cells in the experimental group in the cerebralhemorrhage appeared during6~24h, reached the peak during24~72h, decreasedwhen it was after72h, but significantly higher than those in the control group(P<0.05). TNF-α, IL-1expression of experimental group also began to increase during6~24h, reached the peak during24~72h, decreased when it was after72h, butsignificantly higher than those in the control group (P<0.05). IL-1expression ofexperimental group increased during6~24h,(P<0.05). Then its expression decreasedduring24~72h and>72h, showed a lower levels than those in the control group(P<0.05). Expression of CD163mRNA and CD163protein in the experimental groupbegan to increase during6~24h, still increased when it was after72h, significantlyhigher than those in the control group (P<0.05). Correlation analysis showed that:CD163mRNA and TNF-α, IL-1protein expression were negatively correlated(P<0.01); CD163protein expression and IL-10expression always made a positivecorrelation (P<0.01). Expression of HO-1mRNA and HO-1protein in theexperimental group began to increase during6~24h, still increased when it was after72h, significantly higher than those in the control group (P<0.05). Correlationanalysis showed that: HO-1mRNA and TNF-α, IL-1protein expression werenegatively correlated (P<0.01). Correlation analysis showed that: CD163mRNA andHO-1mRNA, CD163protein and HO-1protein expression were positivelycorrelated (P<0.01). We concluded that perihematoma tissue after CerebralHemorrhage existed inflammation and apoptosis. TNF-α, IL-1and IL-10wereimportant cytokines involved in inflammation of intracerebral hemorrhage.Expression of CD163in human brain tissue in intracerebral hemorrhage increasedsignificantly, and made a negative correlation with TNF-α and IL-1expression,while there is a positive correlation between CD163and IL-10. CD163played animportant role in anti-inflammatory reactions in perihematoma tissue after CerebralHemorrhage. Expression of HO-1in human brain tissue in intracerebral hemorrhageincreased significantly, and made a negative correlation with TNF-α and IL-1expression. HO-1also played an important role in anti-inflammatory reactions inperihematoma tissue after cerebral Hemorrhage. CD163and HO-1expression werepositively correlated and associated in the function promoting each other, and play acoordination work together to form the metabolic pathways of Hb after intracerebralhemorrhage.