Objective The study was to investigate the value of deduction and application of anterior compression index in evaluation of atlantoaxial dislocation and restoration. Method Twenty-eight cases of the control group and 28 cases of atlantoaxial dislocation treated with posterior restoration and screw-rod internal fixation technique before and af?ter surgery were recruited in this study and their data was retrospectively analyzed. All of the people underwent sagittal computerized tomography scan films. The anterior compression index was measured in all cases. Results The mean value of anterior compression index of the control group was 87.86±24.98. The mean value of anterior compression index of the preoperative patients was 230.44 ± 97.60 and the mean value of the postoperative patients was 106.27 ± 73.53. There was significant difference in those two parameters between the preoperative patients and the controls(t=-7.50,P<0.0001). There was no significant difference between the postoperative patients and the control group (t=-1.26, P=0.2171). Anteri?or compression index were significantly lower after surgical operation (t=10.35, compared with before, P<0.0001). Con?clusion Anterior compression index can be an excellent measurement tool for the assessment of relationship of atlas and axis in atlantoaxial dislocation patients before and after posterior restoration operation.

OBJECTIVETo explore the role of P38 signaling pathway in neonatal rat astrocyte swelling and the expression of aquaporin-4 (AQP4) after oxygen-glucose deprivation (OGD) and recovery (OGD/R).

METHODSPrimarily cultured neonatal rat astrocytes were subject to OGD for 5 h followed by oxygen-glucose recovery in the presence or absence of the P38 inhibitor SB203580 (10 µmol/L). The astrocytes were investigated at 0.5, 2, 8 and 24 h after oxygen-glucose recovery for morphological changes and cell injuries using lactate dehydrogenase (LDH) assay. The expressions of P38, P-P38, and AQP4 mRNAs and proteins in the astrocytes were detected using RT-PCR and Western blotting.

RESULTSOGD/R caused significantly enhanced expression of P-P38 protein, and this effect was blocked by SB203580. AQP4 mRNA and protein expression declined transiently at 0.5 h after OGD and increased gradually to reach the peak level at 8 h (P<0.05). Application of the SB203580 significantly lowered OGD-induced AQP4 mRNA and protein up-regulation (P<0.05). Astrocyte swelling occurred after OGD/R but was obviously lessened by SB203580. LDH release increased markedly after OGD/R, and was attenuated by treatment with SB203580 (P<0.01).

CONCLUSIONP38 signaling pathway participates in astrocyte swelling after OGD/R, and blocking this pathway can attenuate AQP4 up-regulation and ameliorate the cell swelling.

Animals ; Animals, Newborn ; Aquaporin 4 ; metabolism ; Astrocytes ; metabolism ; pathology ; Brain Edema ; metabolism ; pathology ; Cell Hypoxia ; Glucose ; pharmacology ; MAP Kinase Signaling System ; physiology ; Oxygen ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism

OBJECTIVETo explore the role of p38 signal pathway in regulating matrix metalloproteinase-9 (MMP-9) expression and brain edema formation in a rat model of traumatic brain injury (TBI).

METHODSA total of 130 adult male Sprague Dawley rats were randomly divided into 4 groups, namely the normal group (n=10), sham-operated group (n=40), TBI (induced by Feeney free falling methods) group (n=40), and SB group with intraperitoneal SB203580 treatment (10 µmol/L) 15 min before TBI (n=40). The rats were sacrificed 2 h and 2 days after TBI. The expressions of p38, p-p38, and MMP-9 mRNA and protein were detected by RT-PCR and Western blotting. The blood brain barrier permeability was detected by Evans Blue (EB) test, and the brain water content (BWC) was determined using a gravimetric technique.

RESULTSThe expression of p-p38 protein increased markedly 2 h after TBI (P<0.05), and was suppressed by SB203580 treatment (P<0.05). MMP-9 mRNA and protein showed no obvious increase at 2 h after TBI, but significantly increased at 2 days as compared with those in the sham-operated group (P<0.05). MMP-9 mRNA and protein were much lower in SB group than in TBI group 2 days after TBI (P<0.05). The blood brain barrier permeability significantly increased 2 h after TBI (P<0.05) and kept increasing until 2 days (P<0.05), but was reduced significantly by SB203580 (P<0.05). BWC increased obviously 2 days after TBI (P<0.05) and was lessened by SB203580 (P<0.05).

CONCLUSIONBlocking p38 signal pathway can attenuate MMP-9 upregulation and brain edema after TBI, suggesting the important role of p38 in regulating MMP-9 expression to affect traumatic brain edema.

Animals ; Brain Edema ; pathology ; Brain Injuries ; metabolism ; Enzyme Inhibitors ; pharmacology ; Imidazoles ; pharmacology ; MAP Kinase Signaling System ; Male ; Matrix Metalloproteinase 9 ; metabolism ; Pyridines ; pharmacology ; Rats ; Rats, Sprague-Dawley

Objective To explore the role of apoptosis signal regulating kinase 1(ASK1) in inflammatory mediated secondary injury after spinal cord injury(SCI) in rats.Methods The rat contusion SCI model was used.Forty-eight rats were randomly divided into the sham operation group(Sham),normal saline(Saline group) and inflammatory factors group (Cytokine group) respectively.The expressions of ASK1 and phosphorylated ASK1(pASK1) were detected by using Western blot.The Basso Beattie Bresnahan (BBB) scores and Grid Walking method were performed to assess the behavior changes of injured rat hindlimbs.Somatosensory evoked potential(SEP) and motor evoked potential(MEP) were used to examine the electrophysiological change.Results The expression levels of ASK1 mRNA and protein had no obvious change at 1 week after SCI;the pASK1 expression level in the Cytokine group was significantly up-regulated compared with the Saline group(P=0.002);the BBB scores at 3 or 4 weeks after SCI in the Cytokine group was significantly decreased compared with the Saline group (P =0.000,P =0.000);the hindlimbs missed step rate at 4 weeks following SCI in the Cytokine group was increased compared with the Saline group (P =0.032);the latent period of SEP and MEP in the Cytokine group was prolonged(P =0.043,P =0.045),while the wave peak value had no obvious changed (P =0.889,P=0.434).Conclusion Inflammatory cytokines may lead the hindlimbs movement dysfunction to be aggravated after SCI in rat,its mechanism may be related with the phosphorylation elevation of ASK1.

OBJECTIVE: To investigate the effects of blocking the activation of ERK pathway on the expression of matrix metalloproteinase-9 (MMP-9) and the formation of cerebral edema in SD rats after brain injury. METHODS: Ninety SD rats were randomly divided into 3 equal groups, including a sham-operated group, modified Feeney's traumatic brain injury model group, and ERK inhibition group where the ERK inhibitor SCH772984 (500 μg/kg) was injected via the femoral vein 15 min before brain trauma. At 2 h and 2 days after brain trauma, the permeability of blood-brain barrier was assessed by Evans blue method, the water content of the brain tissue was determined, and the phosphorylation level of ERK and the expression level of MMP-9 mRNA and protein were measured by RT-PCR and Western blotting. RESULTS: Compared with the sham-operated group, the rats with brain trauma exhibited significantly increased level of ERK phosphorylation at 2 h and significantly increased expression of MMP-9 mRNA and protein 2 days after the injury ( < 0.01). Treatment with the ERK inhibitor significantly decreased the phosphorylation level of ERK after the injury ( < 0.01), suppressed over-expression of MMP-9 mRNA and protein 2 days after the injury ( < 0.01). The permeability of blood-brain barrier increased significantly 2 h after brain trauma ( < 0.05) and increased further at 2 days ( < 0.01); the water content of the brain did not change significantly at 2 h ( > 0.05) but increased significantly 2 d after the injury ( < 0.01). Treatment with the ERK inhibitor significantly lowered the permeability of blood-brain barrier and brain water content after brain trauma ( < 0.01). CONCLUSIONS Blocking the activation of ERK pathway significantly reduced the over-expression of MMP-9 and alleviates the damage of blood-brain barrier and traumatic brain edema, suggesting that ERK signaling pathway plays an important role in traumatic brain edema by regulating the expression of MMP-9.
Animals ; Brain Edema ; drug therapy ; etiology ; Brain Injuries, Traumatic ; complications ; drug therapy ; Gene Expression Regulation, Enzymologic ; drug effects ; Indazoles ; pharmacology ; therapeutic use ; MAP Kinase Signaling System ; drug effects ; Matrix Metalloproteinase 9 ; genetics ; Piperazines ; pharmacology ; therapeutic use ; Protein Kinase Inhibitors ; pharmacology ; therapeutic use ; Random Allocation ; Rats ; Rats, Sprague-Dawley

OBJECTIVE: To investigate the effects of blocking the activation of ERK pathway on the expression of matrix metalloproteinase-9 (MMP-9) and the formation of cerebral edema in SD rats after brain injury. METHODS: Ninety SD rats were randomly divided into 3 equal groups, including a sham-operated group, modified Feeney's traumatic brain injury model group, and ERK inhibition group where the ERK inhibitor SCH772984 (500 μg/kg) was injected via the femoral vein 15 min before brain trauma. At 2 h and 2 days after brain trauma, the permeability of blood-brain barrier was assessed by Evans blue method, the water content of the brain tissue was determined, and the phosphorylation level of ERK and the expression level of MMP-9 mRNA and protein were measured by RT-PCR and Western blotting. RESULTS: Compared with the sham-operated group, the rats with brain trauma exhibited significantly increased level of ERK phosphorylation at 2 h and significantly increased expression of MMP-9 mRNA and protein 2 days after the injury ( < 0.01). Treatment with the ERK inhibitor significantly decreased the phosphorylation level of ERK after the injury ( < 0.01), suppressed over-expression of MMP-9 mRNA and protein 2 days after the injury ( < 0.01). The permeability of blood-brain barrier increased significantly 2 h after brain trauma ( < 0.05) and increased further at 2 days ( < 0.01); the water content of the brain did not change significantly at 2 h ( > 0.05) but increased significantly 2 d after the injury ( < 0.01). Treatment with the ERK inhibitor significantly lowered the permeability of blood-brain barrier and brain water content after brain trauma ( < 0.01). CONCLUSIONS Blocking the activation of ERK pathway significantly reduced the over-expression of MMP-9 and alleviates the damage of blood-brain barrier and traumatic brain edema, suggesting that ERK signaling pathway plays an important role in traumatic brain edema by regulating the expression of MMP-9.
Animals ; Blood-Brain Barrier ; Brain Edema ; Brain Injuries, Traumatic ; MAP Kinase Signaling System ; Matrix Metalloproteinase 9 ; Rats ; Rats, Sprague-Dawley