Research On Serum Soluble TRAIL Level In Patients With Acute Cerebral Infarction And Cerebral Hemorrhage

Background: Cerebral infarction and cerebral hemorrhage are commontypes of acute cerebral vascular disease. Both of them are chief reasons of death and disability with high incidence. Cell apoptosis which plays an important role in neuronal injury after cerebral infarction and cerebral hemorrhage is a chief form of later neuronal death.TRAIL (TNF-related apoptosis inducing ligand) which was identified in 1995 is another member of TNF superfamily and it is highly homologous to Fas gene. It is able to induce apoptosis in cancer cells, virus infective cells and some transformational cells, but has no toxicity to normal cells. In 1999 Ana Martin-Villalba provided evidence that TRAIL expressed in brain tissue and played an important role in neuronal apoptosis after cerebral infarction. Similar to FasL, TRAIL exists its soluble form. It is proved that soluble TRAIL (sTRAIL) can induce apoptosis widely in cells of many resources.The effect of TRAIL in cerebral infarction has been attended. But the level of serum sTRAIL in patients of acute cerebral infarction and the relationship between sTRAIL and cerebral hemorrhage haven't been reported.Objective: To investigate the expression of sTRAIL levels and explore its role in acute phase of cerebral infarction and cerebral hemorrhage. Methods: 45 cases with acute cerebral infarction and 20 cases with acutecerebral hemorrhage were selected. While 20 healthy people served as the control group. And 20 patients belonging to the above cerebral infarction patients from whom consent for blood sampling have the second blood samples 14 days later. The concentrations of serum TRAIL were measured with Enzyme-Linked Immuno Sorbent Assay. Some clinical data of the subjects were recorded, such as sex, age, the scores of CNFDS, the infarct area, the type of stroke.Results: 1. The concentrations of sTRAIL were (115.94 ± 50.25) pg/ml inpatients with cerebral infarction, (60.41 ± 32.97) pg/ml in patients with acute cerebral hemorrhage, and (75.01 ± 31.27) pg/ml in normal control. The concentrations of serum sTRAIL in patients with cerebral infarction were higher than that in normal control (p<0. 05) . And there was no significant difference between the concentrations of sTRAIL in patients with cerebral hemorrhage and that in normal control (p>0. 05) .2. The concentrations of sTRAIL were (110.61±47.46) pg/ml, (121.40± 39.83) pg/ml and (113.68±37.22) pg/ml in acute cerebral infarction patients of varmitus type .There was no significant difference between them (p>0. 05) .3. The concentrations of sTRAIL were (104.21±45.31) pg/ml, (107.98 ± 41.20) pg/ml and (137.11±31.45) pg/ml in patients with small-area, medium-area and large-area cerebral infarction. The concentrations of serum sTRAIL in patients with large-area infarction were higher than that with small-area, medium-area infarction (p<0.05) . And there was no significant difference between the concentrations of serum sTRAIL in patients with small-area and medium-area infarction (p>0.05) .4. The concentrations of sTRAIL were (129.98 ± 41.06) pg/ml, (96. 37± 44.23) pg/ml and (118. 46±38. 41) pg/ml in patients with complete stroke, progressive stroke and RIND. The concentrations of serum sTRAIL in patients with progressive stroke were lower than that with complete stroke and RIND (p<0. 05) . And there was no significant difference between the concentrations of serum sTRAIL in patients with progressive stroke and that with RIND (p>0. 05) .5. The concentrations of sTRAIL were (101.9±31. 14) pg/ml in patients with cerebral infarction on the 14th day. There was no significant difference between the concentrations of sTRAIL in patients with early acute phase and that in late acute phase of cerebral infarction (p>0. 05) . The concentrations of serum sTRAIL in patients with both early and late acute phase of cerebral infarction were higher than that in normal control (p<0.05) .Conclusions: 1. The serum sTRAIL level in the first two weeks ofcerebral infarction was increased.2. The serum sTRAIL level has no relationship with CNDFS but depends on infarction areas. The serum sTRAIL level was higher in patients with large infarction.3. Compared to complete infarction and RIND, The serum sTRAIL level was lower in progressive infarction.4. TRAIL may be involved in the pathophysiological process of cerebral infarction. Interfering in TRAIL way may inhibit neuronal apoptosis. It provides another possible method of treating cerebral infarction.5. The serum sTRAIL level is not changed in cerebral hemorrhage patients.