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High mobility group box 1 (HMGB1) is a classic damage-associated molecular pattern that has an important role in the pathological inflammatory response. In vitro studies have demonstrated that the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway is involved in the regulation of HMGB1 expression, mediating the inflammatory response. Therefore, the purpose of the present study was to evaluate JAK2/STAT3 pathway involvement in the subarachnoid hemorrhage (SAH)-dependent regulation of HMGB1, using an in vivo rat model. A SAH model was established by endovascular perforation. Western blotting, immunohistochemistry and immunofluorescence were used to analyze HMGB1 expression after SAH. In addition, the effects of AG490 after SAH on JAK2/STAT3 phosphorylation, HMGB1 expression and brain damage were evaluated. The results of the present study demonstrated that JAK2/STAT3 was significantly phosphorylated (P<0.05) and the total HMGB1 protein level was significantly increased (P<0.05) after SAH. In addition, the cytosolic HMGB1 level after SAH demonstrated an initial increase followed by a decrease to the control level, while the nuclear HMGB1 level after SAH demonstrated the opposite trend, with an initial decrease and subsequent increase. AG490 administration after SAH significantly inhibited JAK2/STAT3 phosphorylation (P<0.05), suppressed the expression and translocation of HMGB1, reduced cortical apoptosis, brain edema and neurological deficits. These results demonstrated the involvement of the JAK2/STAT3 pathway in HMGB1 regulation after SAH. [ABSTRACT FROM AUTHOR]

Ischemic postconditioning refers to controlling reperfusion blood flow during reperfusion after ischemia, which can induce an endogenous neuroprotective effect and reduce ischemia-reperfusion injury. Activation of endogenous neuroprotective mechanisms plays a key role in protecting against brain ischemia-reperfusion injury. The mechanisms of cerebral ischemic postconditioning are not completely clear, and the following aspects may be involved: downregulation of oxidative stress, attenuating mitochondrial dysfunction, attenuating endoplasmic reticulum stress, accelerating the elimination of glutamate, increasing rCBF, inhibiting apoptosis, inhibiting autophagy, and regulating signal transduction. [ABSTRACT FROM AUTHOR]

Objective To clarify the effect of cortical spreading depression (CSD) on cortical cerebral blood flow and apoptosis following subarachnoid hemorrhage (SAH) in rats. Methods SAH was induced in male Wistar rats by autologous blood injection into the cisterna magna and CSD was induced in rats with KCl. The cortical blood flow was measured by laser Doppler flowmeter and apoptosis were detected by TUNEL staining. Results In SAH groups the cortical cerebral blood flow was significantly reduced and cortical cell apoptosis was increased compared with those in blank and normal saline groups. After CSD, the cortical cerebral blood flow and apoptosis in SAH groups were more obvious than in blank and normal saline groups. Conclusion CSD can reduce cortical cerebral blood flow and aggravate apoptosis after SAH. It may be one of the mechanisms of delayed ischemic neurologic deficit. [ABSTRACT FROM AUTHOR]

Objective To study the role of neuropeptide Y (NPY) in vasospasm after subarachnoid hemorrhage (SAH) in vitro cultured rat cerebral vascular smooth muscle cells (VSMCs) by observing the proliferation and contraction protein expression of VSMCs. Methods Male or female SD rats weighing 150 g were killed by blood loss. After infusion with saline, the circle of Willis artery and its branches were harvested and primary VSMCs were cultured. Then in vitro model of SAH was established by exposure to oxyhemoglobin of 10-6 mol/L. Then the cells were treated with NPY or BIB03304 (a commonly used blocker of NPY receptor), or NPY + BIB03304. After culturing 1,3,5 and 7 days, immunofluorescence was used to measure the expression of α-actin. IPP software was used to measure the fluorescence intenty and SPSS16.0 statistical software was used for data analysis. Results VSMCs were successfully cutured whli digettion method. The fifth generation of visible cells showed a typical "valley-peak"-like growth. In NPY and NPY + SAH groups, 3-day cell intervention significantly increased the fluorescence intensity of α-actin (P<0. 05), while BIBO 3304 treatment reduced the expression of α-actin, the intensity of which was as weak as that of the blank group (P>0.05). Conclusion NPY increases α-actin expression in VSMCs while BIBO 3304 blocks the up-regulation of α-acin by NPY. NPY plays an important role in delayed cerebral vasospasm after SAH. [ABSTRACT FROM AUTHOR]

Objective To investigate changes of AdipoR in the central nervous system and concentration of serum adiponectin after subarachnoid hemorrhage (SAH) in rats. Methods Fifty-four male Sprague-Dawley rats were randomly divided into three groups: normal group (n = 12), sham-operation group(n = 12), and SAH model group (n = 30). An endovascular perforation model was used to induce SAH in the rats. The expression of AdipoR in the central nervous system was detected by Western blot. The concentration of serum adiponectin was detected by ELISA. Results Compared with that in normal group and sham-operation group, the concentration of serum adiponectin was decreased signíficantly at day 1, 2 and 3 after SAH (P<0.05). Compared with that in normal group and sham-operation group, the expression of AdipoR1 in the cerebral cortex and the hippocampus was up-regulated sharply after SAH (P<0.05), but the expression of AdipoR2 did not change significantly (P>0.05). Conclusion Adiponectin may be involved in the pathophysiological process of early brain injury after SAH. The decreased concentration of serum adiponectin and the up-regulation of AdipoR1 expression are both important pathological mechanisms leading to early brain injury after SAH. [ABSTRACT FROM AUTHOR]

Objective To investigate the possible role of canonical trasnient receptor potential channels (TRPCs) in calcium overload of neurons after subarachnoid hemorrhage (SAH) and discuss the mechanism of TRPCs involved in delayed neuronal death (DND) after SAH. Methods Rat models of SAH were established by double-blood injection via the citerna magna. SAH intervention group was established by using SKF96365 intracerebroventricular injection. Intracellular calcium concentration was detected by Fura-2AM. The dynamic expressions of TRPCs in the cortex and basilar artery were determined by Western blot. The mRNA levels of TRPCs in the cortex and basilar artery were determined by RT-PCR. The results were compared with those in DMSO control model group, saline control group and normal group. The apoptosis of cortical neurons was detected by TUNEL. One-way ANOVA was used to compare within each group. Results The protein expressions and mRNA levels of TRPC1 in the cortex and the basilar artery continuourly increased after SAH and reached the peak on day 5 while intracellular calcium concentration and TUNEL-positive cell counts also reached the peak. After injection of SKF96365, a TRPCs blocker, the protein expressions and mRNA levels of TRPC1 were inhibited, intracellular calcium concentration and TUNEL-positive cell counts decreased. Meanwhile, the scores of rat neurological functions were improved. The expressions of TRPC3 in the cortex and the basilar artery showed no significant change. Conclusion TRPC1 induced calcium overload and CVS after SAH are the major causes of delayed neuronal death. Suppressing calcium influx induced by TRPC1 could delay neuronal death and improve neurological functions. [ABSTRACT FROM AUTHOR]

Objective To explore the dynamic expression of high mobicity group protein B1(HMGB1) in rats brain tissue after subarachnoid hemorrhage (SAH) and its significance. Methods Rats SAH models were established by perforation of anterior cerebral artery, and randomly divided into 5 subgroups (control group, 6 h, 1, 3, 7 d). ELISA was used to determine the plasm HMGB1 levels after SAH; immunohistochemical staining and western blot were used to survey the dynamic expression of HMGB1 in brain tissue after SAH. Results Plasm HMGB1 levels significantly increased after SAH, and continued to rise from 6 hto 7 d. Immunohistochemical staining indicated that HMGB1 positive cells significantly decreased within the brain tissue in early stage (6 h, 1 d) after SAH, in late stage (3, 7 d) it began to rise and translocated to cytoplasm; Western blot results also showed the expression of HMGB1 decreased first and then increased in the frontal lobe cortex after SAH. Conclusion HMGB1 expression significantly increased not only in brain tissue but also in plasma. HMGB1 may play a important role in inflammatory brain damage after SAH. [ABSTRACT FROM AUTHOR]

Early brain injury (EBI) and delayed cerebral injury following subarachnoid hemorrhage (SAH) are closely associated with poor prognois in patients. Studies on the molecular mechanisms of EBI have revealed several pathological mechanisms involved in neurovascular dysfunction. These mechanisms include microvascular changes, altered ionic homeostaiis, blood-brain barrier disruption, inflammation, oxidative stress, and cell death pathway activation. These studies also provide multiple possible intervention targets for protecting neurological function after SAH, in which calcium channel blockers, endothelin-1 antagonism, anti-platelet agents, anti-inflammatory agents, and antioxidants may have neuroprotective effects agaimt EBI. Further elaborating on the molecular mechanisms of SAH-induced hypoxic-ischemic brain injury, neuroinflammation, cortical spreading depression, neuronal cell death and revealing the evolvement of these complex pathophysiological proceises are of great significance for reducing brain injury after SAH, promoting nerve repair, and ameliorating patients' quahty of life and overall mortahty. [ABSTRACT FROM AUTHOR]

Objective To investigate the trends of peripheral blood leucocyte counts and MMP-9/TIMP-1 ratio in acute experimental subarachnoid hemorrhage model in rats and their relationship wíth early brain injury. Methods A rat single cisterna magna injection model was used. Leukocytes were counted by blood counting chamber, and MMP-9 and TIMP-1 were measured by ELISA. The dry-wet weight method was used to measure brain water content. The inside diameter was measured on an HE stained basilar artery. Results The brain water content increased significantly at 6 h after subarachnoid hemorrhage and peaked at 24 h, so did the leukocyte count as well as MMP-9 and TIMP-1 contents. Both the leukocyte count and MMP-9/TIMP-1 ratio were related to early brain injury after subarachnoid hemorrhage. Conclusion The leukocyte count and MMP-9/TIMP-1 ratio increase significantly in the early stage of subarachnoid hemorrhage and return to normal after 72 h. The trend is related to early brain injury after subarachnoid hemorrhage. The MMP-9/TIMP-1 ratio may be used as a predictor of the appearance of early brain injury. [ABSTRACT FROM AUTHOR]

Objective To investigate the activation of necroptosis pathway and explore the role and molecular mechanism of necroptosis in early brain injury after subarachnoid hemorrhage (SAH). Methods Forty adult male SD rats were divided into four groups ( n = 10 in each): sham, SAH, and SAH treatment plus Nec-1 or dimethyl sulfoxide (DMSO) . SAH model was established by endovascular perforation technique. In SAH+Nec-1 and SAH+ DMSO groups, Nec-1 or DMSO was injected intracerebroventsicularly 30 min prior to SAH establishment. Animals were then sacrificed at 24 h after modeling in each group. The neurological severity scores and brain water content were determined; immunohistochemical method was used in detecting the expression of receptor interacting protein 3 (RIP3). Results Neurological dysfunction, the number of necrotic neuronal cells, brain water content and the expression of RIP3 were significantly increased in the brain tissues of SAH rats (P<0.01). Neurological dysfunction, the number of necrotic neuronal cells, brain water content and the expression of RIP3 were significantly reduced after Nec-1 treatment (P<0.01). Conclusion Necroptoiis is activated and involved in the pathophysiological mechanism of early brain injury after SAH. RIP3 may play a crucial role in necroptosis pathway. Inhibiting necroptosis may be of great importance for protecting neuronal cells and reducing edema in early brain injury after SAH. [ABSTRACT FROM AUTHOR]

Objective To investigate the possible role of store-operated calcium channels (SOCC) in early brain injury (EBI) after subarachnoid hemorrhage (SAH) and to explore the relationship between SOCC and calcium overload induced delayed neuronal death (DND) after SAH. Methods Rabbits models of SAH were established using the single-blood injection method via the cisterna magna. SAH intervention group was established by intracerebroventricular injection of 2-aminoethyldiphenyl borate (2-APB). Intracellular calcium concentration was detected by Fura-2AM. The dynamic expression of SOCC was determined by Western blot. The apoptosis of cortical neurons was detected by TUNEL. One-way ANOVA was used to compare between experimental, normal control and sham-operation groups. Results The protein expressions of STIM1 and ORAI1 in the cortex increased continuously after SAH and reached the peak at day 3; intracellular calcium concentraron also reached the peak. After injection of SOCC blocker, the protein expressions of STIM1 and ORAI1 were inhibíted and intracellular calcium concentration decreased. Meanwhile, the scores of neurological functions. [ABSTRACT FROM AUTHOR]

Objective To explore the effects of necrostatin-1 on cortical necroptosis, autophagy and necrosis after subarachnoid hemorrhage (SAH). Methods Totally 72 SD rats were randomly divided into sham operation group, model group, vehicle group and necrostatin-1 group. Rats in vehicle group were given 2 μL of dimethyl sulfoxide by intracerebroventricular injection while those in necrostatin-1 group were given 5.2 μg of necrostatin-1 dissolved in 2 μL of dimethyl suboxide. Subarachnoid hemorrhage models were induced by intravascular puncture. In each group 9 rats were used to observe the expressions of receptor interacting protein 3 and microtubule associated protein 1 light chain 3 in the cerebral cortex by Western blot; 9 rats were injected intraperitoneally with propidium iodide to observe necroiis in each group. Loeffler neurological score was recorded for all rats at 6, 12 and 24 h. Results Necrostatin-1 suppressed receptor interacting protein 3 and microtubule associated protein 1 iight chain 3 in the cerebral cortex (P<0.05), decreased the number of propidium iodide positive celis in the cortex (P<0.05), and improved Loeffler neurological scores at 12 and 24 h (P<0.05), which showed that necrostatin-1 could improve the prognosis after SAH. Conclusion Necrostatin-1 might suppress the level of autophagy and necrosis when inhibiting post-SAH necroptosis in cerebral cells. [ABSTRACT FROM AUTHOR]

Objective To investigate the activation of AMP-activated protein kinase (AMPK) and Bim in rat cortex after subarachnoid hemorrhage (SAH) and to explore the role of AMPK in cortical apoptosis in early brain injury after SAH. Methods SAH model was established by an endovascular perforation technique. The immunohistochemical method was used to detect the localization of AMPK and phosphorylated AMPK. RT-PCR was performed to detect the dynamic mRNA expression of AMPKα, and Western blot was used to detect the protein leveis of phosphorylated AMPK and apoptosis-related proteins (Bim and caspase-3) in the cortex. After AICAR and compound C were administered via i. c. v, the change of p-AMPK level was examined, and the effects of AICAR and compound C on neurological behavior and apoptosis-related protein expressions were observed. Results Experimental SAH increased the expressions of AMPKα mRNA and phosphorylated AMPK. Bim and caspase-3 were also significantiy increased. Wth compound C treatment, the phosphorylation level of AMPK and the up-regulation of Bim were modfied. However, AICAR administration exacerbated cortical apoptosis and neurological deficit through up-regulation of Bim. Conclusion AMPK is involved in the pathophysiological process of neuronal apoptosis in early brain injury after SAH. The mechanism may be related to the regulation of transcription of Bim. Inhibition of AMPK signaling pathway can provide neuroprotection by reducing cortical apoptosis after SAH. [ABSTRACT FROM AUTHOR]

Tissue plasminogen activator is usually used for the treatment of acute ischemic stroke, but the role of endogenous tissue plasminogen activator in traumatic brain injury has been rarely reported. A rat model of traumatic brain injury was established by weight-drop method. The tissue plasminogen activator inhibitor neuroserpin (5 μL, 0.25 mg/mL) was injected into the lateral ventricle. Neurological function was assessed by neurological severity score. Neuronal and axonal injuries were assessed by hematoxylin-eosin staining and Bielschowsky silver staining. Protein level of endogenous tissue plasminogen activator was analyzed by western blot assay. Apoptotic marker cleaved caspase-3, neuronal marker neurofilament light chain, astrocyte marker glial fibrillary acidic protein and microglial marker Iba-1 were analyzed by immunohistochemical staining. Apoptotic cell types were detected by immunofluorescence double labeling. Apoptotic cells in the damaged cortex were detected by terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP-biotin nick-end labeling staining. Degenerating neurons in the damaged cortex were detected by Fluoro-Jade B staining. Expression of tissue plasminogen activator was increased at 6 hours, and peaked at 3 days after traumatic brain injury. Neuronal apoptosis and axonal injury were detected after traumatic brain injury. Moreover, neuroserpin enhanced neuronal apoptosis, neuronal injury and axonal injury, and activated microglia and astrocytes. Neuroserpin further deteriorated neurobehavioral function in rats with traumatic brain injury. Our findings confirm that inhibition of endogenous tissue plasminogen activator aggravates neuronal apoptosis and axonal injury after traumatic brain injury, and activates microglia and astrocytes. This study was approved by the Biomedical Ethics Committee of Animal Experiments of Shaanxi Province of China in June 2015., Competing Interests: None

The role of vascular endothelial growth factor A in platelet adhesion in cerebral microvessels in the early stage of subarachnoid hemorrhage remains unclear. In this study, the endovascular puncture method was used to produce a rat model of subarachnoid hemorrhage. Then, 30 minutes later, vascular endothelial growth factor A antagonist anti-vascular endothelial growth factor receptor 2 antibody, 10 μg, was injected into the right ventricle. Immunohistochemistry and western blot assay were used to assess expression of vascular endothelial growth factor A, occludin and claudin-5. Immunohistochemical double labeling was conducted to examine co-expression of GP Ia-II integrin and type IV collagen. TUNEL was used to detect apoptosis in the hippocampus. Neurological score was used to assess behavioral performance. After subarachnoid hemorrhage, the expression of vascular endothelial growth factor A increased in the hippocampus, while occludin and claudin-5 expression levels decreased. Co-expression of GP Ia-II integrin and type IV collagen and the number of apoptotic cells increased, whereas behavioral performance was markedly impaired. After treatment with anti-vascular endothelial growth factor receptor 2 antibody, occludin and claudin-5 expression recovered, while co-expression of GP Ia-II integrin and type IV collagen and the number of apoptotic cells decreased. Furthermore, behavioral performance improved notably. Our findings suggest that increased vascular endothelial growth factor A levels promote platelet adhesion and contribute to early brain injury after subarachnoid hemorrhage. This study was approved by the Biomedical Ethics Committee, Medical College of Xi'an Jiaotong University, China in December 2015., Competing Interests: None

Rosiglitazone up-regulates caveolin-1 levels and has neuroprotective effects in both chronic and acute brain injury. Therefore, we postulated that rosiglitazone may ameliorate diffuse axonal injury via its ability to up-regulate caveolin-1, inhibit expression of amyloid-beta precursor protein, and reduce the loss and abnormal phosphorylation of tau. In the present study, intraperitoneal injection of rosiglitazone significantly reduced the levels of amyloid-beta precursor protein and hyperphosphorylated tau (phosphorylated at Ser(404)(p-tau (S(404))), and it increased the expression of total tau and caveolin-1 in the rat cortex. Our results show that rosiglitazone inhibits the expression of amyloid-beta precursor protein and lowers p-tau (S(404)) levels, and it reduces the loss of total tau, possibly by up-regulating caveolin-1. These actions of rosiglitazone may underlie its neuroprotective effects in the treatment of diffuse axonal injury.

Aim: The role of statins for treating aneurysmal subarachnoid hemorrhage (aSAH) remains uncertain. In this study, the relevance of different end points was evaluated in order to clarify the action and efficacy of statins., Material and Methods: A systematic literature retrieval was carried out to obtain randomized controlled trials (RCTs) from before March 2013 on the use of statins for aSAH. Data extraction and quality evaluation of the studies were performed by 2 investigators. A meta-analysis was performed using Review Manager (RevMan) software version 5.2.3., Results: Seven randomized controlled trials comprising 347 patients that met the inclusion criteria were included in this meta-analysis. Results showed that, in aSAH, statins did not reduce vasospasm on transcranial Doppler (RR=0.80; 95% CI, 0.53-1.21; p=0.29) or improve outcomes (RR=0.92; 95% CI, 0.71-1.20; p=0.54). However, statins were able to decrease delayed ischemic neurological deficits (RR=0.56; 95% CI, 0.41-0.75; p=0.0001) and mortality (RR=0.54; 95% CI, 0.32-0.91; p=0.02) compared with placebo., Conclusion: Acute statin treatment might not be a good choice for cerebral vasospasm after aSAH. Further large-scale, well-designed RCTs on this topic are still needed.

Objective: To discuss the relationship between the expression of endothelin receptor A (ETRA) in brain tissue and delayed neurological deficit (DND) after subarachnoid hemorrhage (SAH)., Methods: Thirty-one Japanese rabbits were divided into SAH group (n=15), saline group (n=10), puncture group (n=3), normal control group (n=3) randomly, and they subdivided into 1 hour, 3 days, 5 days, 7 days, 10 days subgroups in both SAH group and saline group. The SAH model was successfully reproduced by intracisternal injection of autologous arterial blood twice. When the animals were sacrificed by perfusion, brain stems were harvested and prepared for immunohistochemical staining and hematoxylin and eosin (HE) staining. The pathological changes in the brain tissue were observed with light microscope. Then positive-cell counting was used to semi-quantitative analysis., Results: The expression of ETRA was not detected nearly in neurons or gliocyte either in puncture group (10.6+/-3.9) or in normal group (10.0+/-2.8), while it was detected in some cells in saline group. But no significant difference was showed among the subgroups in saline group (12.3+/-2.1 lowest vs. 13.3+/-2.6 highest, P>0.05) by variance analysis. The expression of ETRA in SAH group was slightly stronger after 1 hour (20.1+/-3.5), peaked at 3 days (48.8+/-6.7), and became weak gradually after 5 days. The ETRA positive cells at 5 days, 7 days, and 10 days were 23.1+/-2.9, 22.5+/-4.2 and 19.1+/-2.8 respectively. There were significant differences among the values at different time points (P<0.05) in SAH group, and the positive cells of ETRA were obviously increased in number in SAH group at all time points compared with saline group (all P<0.05)., Conclusion: ETRA is expressed distinctly in the brain tissue, and it may play an important role in DND pathogenesis.

Objective: To discuss the effect of drainage of the cerebrospinal fluid (CSF) at acute period after aneurysmal subarachnoid hemorrhage (SAH) on the formation of hydrocephalus., Methods: Eighty-four patients with aneurysmal SAH were randomly divided into two groups according to therapeutic regimen. Forty-two cases in specific treatment group were given intravascular embolism at the acute period of hemorrhage after a ruptured aneurysm, then CSF was drained immediately. Forty-two cases were in conventional expectant treatment group. Clinical data and incidence of hydrocephalus of specific treatment group and conventional expectant treatment group were analyzed., Results: Clinical data did not show any differences between two groups, so they could be compared (all P>0.05). The incidence rate of acute hydrocephalus in specific treatment group was 7.14% (3/42 cases), that of subacute hydrocephalus was 4.76% (2/42 cases), and that of chronic hydrocephalus was 16.67% (7/42 cases). The total incidence rate was 28.57%. In conventional expectant treatment group, the incidence rate of acute hydrocephalus was 23.81% (10/42 cases), incidence of subacute hydrocephalus was 9.52% (4/42 cases), and that of chronic hydrocephalus was 35.71% (15/42 cases), and total incidence rate was 69.05%. There was significant difference between specific treatment group and conventional expectant treatment group in incidence of acute and chronic hydrocephalus (acute chi (2)=4.46, chronic chi (2)=3.94, both P<0.05), and there was no difference in subacute hydrocephalus between two groups (chi (2)=0.72, P>0.05), but significant difference was found in total incidence rate between two groups (chi (2)=13.77, P<0.01)., Conclusion: Embolization of the intracranial aneurysm with interventional treatment at the acute hemorrhage stage (within 7 days) for the aneurysmal SAH, followed by immediate drainage of CSF can prevent hydrocephalus or alleviate hydrocephalus, and the treatment plays a significant role in the formation and development of hydrocephalus.

Objective: To discuss the early diagnostic methods and therapeutic principles of aneurysmal subarachnoid hemorrhage (SAH), and evaluate the therapeutic efficacy objectively., Methods: Using neuro-imaging examinations combined with case history and clinical symptoms to make the early diagnosis of 96 case with aneurysmal SAH, and Guglielmi detachable microcoil (GDC) was utilized for early intracapsular embolization in the ruptured aneurysms. Efficient symptomatic treatment was done early after operation., Results: All of 96 cases were early diagnosed and successfully embolized; Among them, the aneurysmal lumen was 100% occluded in 83 cases, 95% in 8 cases, 90% in 5 cases. There were 3 cases complicating with aneurysms rupture during operation, 5 cases with cerebral vasospasm. One case was affected by microcoil terminal escape after operation, 3 recurrent cases were all cured with secondary GDC embolization. There were 9 complications associated with embolization techniques and 13 cases (13.5%) occurring permanent sequelae associated with SAH. According to the Glasgow prognosis score, 77 patients got grade I, 7 grade II, 6 grade III, 3 grade IV, and 3 grade V. The mortality rate was 3.1%., Conclusions: To make early etiological diagnosis of the SAH patients, using GDC to embolize the aneurysms, and earlier efficient symptomatic treatment are important methods to improve the curative rate and reduce the mortality rate.