| Objective:Brain hemorrhage is common and frequently-occurring disease in Nervous system, its morbidity and mortality rates are high, seriously affecting human health and the patient's quality of life. In recent years, Inflammatory reaction in secondary injury after intracerebral hemorrhage in the role of more and more attention, And that it may lead to brain hemorrhage cell apoptosis. At present the mechanism of inflammation after intracerebral hemorrhage is still not very clear. In recent years, Study found the complement system in brain injury inflammation plays an important role. Complement component C3 in the complement of the highest concentrations are two ways to activate the intersection and complement the core hub of the role played by biology, And thus determine the whereabouts of complement C3 can be fully reflected in the activation of complement function and state; Serum apolipoprotein levels to predict cardiovascular and cerebrovascular diseases and diabetes, a better indicator. Apolipoprotein J (apolipoprotein J, Apo J, also known as Clusterin) is a newly discovered a new type of apolipoprotein and a multifunctional glycoprotein, Almost all types of cells can secrete this protein, and there are all the fluids in the body, the highest concentration in the brain; There are many studies have shown that apolipoprotein J involved in many physiological functions, including apoptosis, complement regulation, protection of cell membrane, cell-cell and cell matrix interactions and stability, DNA repair and carcinogenic effects. The experiment by testing experimental cerebral hemorrhage around the corresponding parts of the brain lesions of apolipoprotein-J (Apo-J) mRNA expression levels of the development law After that, Analysis of the expression level of Apo-JmRNA complement C3mRNA with the existence of correlation, and analysis of the expression level of Apo-J mRNA and brain edema (brain water content) whether there is relevance, Apo-J to explore the pathophysiology of cerebral hemorrhage in the course of the mechanism, and explore the course of their disease, the molecular biological mechanisms, in order to find a better basis for treatment. Methods:Evenly divided male and female SD rats 150 weighing 300-350g, were randomly divided into control group, sham operation group and 3 h after cerebral hemorrhage group,6 h group,12 h group, 1d group,3d group,5d group and 7d groups, n= 10. In the stereotactic frame used under autologous arterial blood into the caudate nucleus Preparation of intracerebral hemorrhage model. In the mold after 3h, 6h,12h, 1d,3d,5d,7d 7 time points animals were killed,By dry weight measurement of brain water content (BWC); for ICH group of neurological deficit score; RT-PCR assay ApoJmRNA and complement C3mRNA expression. SPSS 17.0 statistical package with all the information for statistical analysis, data of "mean±standard deviation" means, p＜0.05 for the differences exist,p＞0.05 for the difference does not exist. Results:1. cerebral hemorrhage group each observation time point neurological score was significantly lower than sham operation group (P＜0.05), cerebral hemorrhage group disease score was lowest at 3d.2. cerebral hemorrhage observed in brain water content in each time point and the normal group and the sham group, P＜0.05, with statistically significant; other brain water content at different time points significantly lower than the 3d group, compared P＜0.05, with statistically significance; 3.①normal brain tissue shows low levels of expression C3mRNA;②cerebral hemorrhage was significantly higher than the normal group and sham operation group (P＜0.05), with statistically significant; in which expression of 3d group C3mRNA highest the other time points compared with the 3d group (P＜0.05), with statistically significant.4.①normal brain tissue shows low levels of expression of Apo-JmRNA;②cerebral hemorrhage was significantly higher than the normal group and sham operation group (P＜0.05), statistically significant; 3d group of which the highest expression of Apo-JmRNA, the other time points and the 3d group (P＜0.05), with statistical significance.5. ICH disease score of each group in each group with the corresponding water content of brain tissue around the hematoma was a negative correlation (r=-0.6603, P＜0.05); 6, cerebral hemorrhage model operated side C3 mRNA expression in brain water content value and a positive correlation between (R= 0.758, P＜0.05); 7, cerebral hemorrhage model operated side ApoJ mRNA expression in brain water content value and a positive correlation between (R= 0.702, P＜0.05); 8. intracerebral hemorrhage model operated side ApoJ mRNA expression in the expression of values and C3mRNA positive correlation between the values (R = 0.908, P＜0.05).Conclusion:1. cerebral hemorrhage increased expression of complement C3mRNA, and the degree of brain edema was a positive correlation, suggesting the activation of the complement system, complement system may be involved in cerebral hemorrhage cerebral edema formation and neuronal damage.2. cerebral hemorrhage increased expression of Apo-JmRNA, peak at day 3. And was positively correlated with C3mRNA expression, suggesting that Apo-J may inhibit complement activation, is to play the role of endogenous stress protection.
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