OBJECTIVETo explore the relationship between expression thange of P-selectin after brain injury and secondary brain damage.

METHODSSixty SD rats were randomized into 3 equal groups, namely the control group, mild injury group and severe injury group and animal models of brain injury were established in SD rats according to the method of Feeney. P-selectin expression in the brain tissues were determined at 6 h and l, 3, and 7 days following brain injury (n=5 for each time point). Imaging analysis was performed using computerized imaging technique.

RESULTSP-selectin expression and neutrophil infiltration in the brain tissues increased significantly 6 h after brain injury (P<0.05), reaching the peak level at postoperative 24 h and then gradually decreased.

CONCLUSIONP-selectin expression and neutrophil infiltration increase significantly following brain injury, and the time course and distribution of P-selectin expression are consistent with the secondary damage of the brain, strongly suggesting the involvement of P-selectin upregulation in the secondary insult after brain injury.

Animals ; Brain Chemistry ; Brain Injuries ; etiology ; metabolism ; pathology ; Female ; Immunohistochemistry ; P-Selectin ; biosynthesis ; Random Allocation ; Rats ; Rats, Sprague-Dawley

Early brain injury (EBI) plays a key role in the pathogenesis of subarachnoid hemorrhage (SAH). This study investigated the role of glucose-regulated protein 78 (GRP78) in EBI after SAH. Male Sprague-Dawley rats (n=108) weighing 260±40 g were divided into control, sham-operated, and operated groups. Blood was injected into the prechiasmatic cistern of rats in the operated group. Neurological scores, ultrastructures of neurons, apoptosis, and GRP78 expression in the hippocampus were examined using Garcia scoring system, transmission electron microscopy, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling, and Western blotting at 1, 6, 12, 24, 48, and 72 h after SAH, respectively. The results showed that neurological scores were significantly decreased in the operated group as compared with those in control and sham-operated groups at 12, 24, 48, and 72 h. Metachromatin, chromatin pyknosis at the edge, endoplasmic reticulum swelling, and invagination of nuclear membrane were observed at 24 h in the operated group, indicating the early morphological changes of apoptosis. The number of apoptotic cells was significantly increased in the operated group as compared with that in control and sham-operated groups at 6, 12, 24, 48, and 72 h. The GRP78 protein expression levels in the operated group were significantly elevated at all time points and reached the peak at 12 h. GRP78 expression was positively associated with apoptosis cells and negatively with neurological scores. In conclusion, EBI was demonstrated to occur after SAH and GRP78 was involved in the development of EBI after SAH.
Animals ; Apoptosis ; Brain Injuries ; complications ; metabolism ; pathology ; Chromatin ; pathology ; Endoplasmic Reticulum Stress ; Heat-Shock Proteins ; genetics ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Subarachnoid Hemorrhage ; etiology ; metabolism ; pathology

The expression of vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF)2 in the irradiated brain was examined to test how a single high dose radiation, similar to that used for intraoperative radiation therapy given to the normal cerebrum, can affect the vascular endothelium. After a burr hole trephination in the rat skull, the cerebral hemisphere was exposed to a single 10 Gy dose of gamma rays, and the radiation effect was assessed at 1, 2, 4, 6, and 8 weeks after irradiation. His-tological changes, such as reactive gliosis, inflammation, vascular proliferation and necrosis, were correlated with the duration after irradiation. Significant VEGF and FGF2 expression in the 2- and 8-week were detected by enzyme-linked immunosorbent assay quantification in the radiation group. Immunohistochemical study for VEGF was done and the number of positive cells gradually increased over time, compared with the sham operation group. In conclusion, the radiation injuries consisted of radiation necrosis associated with the expression of VEGF and FGF2. These findings indicate that VEGF and FGF2 may play a role in the radiation injuries after intraoperative single high-dose irradiation.
Animals ; Brain/metabolism/pathology/radiation effects ; Brain Injuries/etiology/*metabolism/*pathology ; Fibroblast Growth Factor 2/*metabolism ; Necrosis ; Radiation Injuries/*pathology ; Radiosurgery/*adverse effects ; Rats ; Rats, Sprague-Dawley ; Up-Regulation/radiation effects ; Vascular Endothelial Growth Factor A/*metabolism

OBJECTIVETo characterize the expression of aquaporin-4 (AQP4), one of the aquaporins (AQPs), in human brain specimens from patients with traumatic brain injury or brain tumors.

METHODSNineteen human brain specimens were obtained from the patients with traumatic brain injury, brain tumors, benign meningioma or early stage hemorrhagic stroke. MRI or CT imaging was used to assess brain edema. Hematoxylin and eosin staining were used to evaluate cell damage. Immunohistochemistry was used to detect the AQP4 expression.

RESULTSAQP4 expression was increased from 15 h to at least 8 d after injury. AQP4 immunoreactivity was strong around astrocytomas, ganglioglioma and metastatic adenocarcinoma. However, AQP4 immunoreactivity was only found in the centers of astrocytomas and ganglioglioma, but not in metastatic adenocarcinoma derived from lung.

CONCLUSIONAQP4 expression increases in human brains after traumatic brain injury, within brain-derived tumors, and around brain tumors.

Adult ; Aged ; Aged, 80 and over ; Aquaporin 4 ; Aquaporins ; metabolism ; Biomarkers ; metabolism ; Brain Edema ; etiology ; metabolism ; pathology ; Brain Injuries ; complications ; metabolism ; pathology ; Brain Neoplasms ; complications ; metabolism ; pathology ; Female ; Humans ; Male ; Middle Aged ; Tissue Distribution

OBJECTIVETo study the correlation between brain edema, elevated intracranial pressure (ICP) and cell apoptosis in traumatic brain injury (TBI).

METHODSIn this study, totally 42 rabbits in 7 groups were studied. Six of the animals were identified as a control group, and the remaining 36 animals were equally divided into 6 TBI groups. TBI models were produced by the modified method of Feeney. After the impact, ICP of each subject was recorded continuously by an ICP monitor until the animal was sacrificed at scheduled time. The apoptotic brain cells were detected by an terminal deoxynucleotide-transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) assay. Cerebral water content (CWC) was measured with a drying method and calculated according to the Elliott formula. Then, an analysis was conducted to determine the correlation between the count of apoptotic cells and the clinical pathological changes of the brain.

RESULTSApoptotic cell count began to increase 2 h after the impact, and reached its maximum about 3 days after the impact. The peak value of CWC and ICP appeared 1 day and 3 days after the impact, respectively. Apoptotic cell count had a positive correlation with CWC and ICP.

CONCLUSIONSIn TBI, occurrence of brain edema and ICP increase might lead to apoptosis of brain cells. Any therapy which can relieve brain edema and/or decrease ICP would be able to reduce neuron apoptosis, thereby to attenuate the secondary brain damage.

Animals ; Apoptosis ; Brain Edema ; etiology ; metabolism ; pathology ; Brain Injuries ; complications ; pathology ; physiopathology ; Cell Count ; Disease Models, Animal ; In Situ Nick-End Labeling ; Intracranial Hypertension ; etiology ; pathology ; physiopathology ; Male ; Necrosis ; genetics ; pathology ; Rabbits ; Reference Values ; Telencephalon ; metabolism ; Water ; metabolism

OBJECTIVETo explore the features of rats organs functional changes after femur shaft fracture combined with brain injury through testing biochemical indicators in rats.

METHODSThirty 4-month-old male SD rats, weight (280 +/- 10) g, were divided into 5 groups according to random number table involving normal control group, at the 1st day of injured group, the 2nd day injured group, the 3rd day injured group, the 5th day injured group, the 7th day injured group, 5 rats in each group. The animal injury model of right femur shaft fracture combined with brain injury were made by instruments in 5 injured groups. At the 1st, 2nd, 3rd, 5th, 7th day after made model, the biochemical indicators of blood serum from abdominal aorta including AST, ALT ,Cr, BUN, LDH and CK were detected and compared.

RESULTSThe biochemical indicator of blood serum (AST, ALT, Cr, BUN, LDH, CK) changed significantly among different groups. AST, ALT, BUN and CK reached peaks at the 1st day after injured (P<0.05). Cr reached peaks at the 3rd day after injured (P<0.05). LDH reached peak at the 2nd day after injured (P<0.05).

CONCLUSIONAfter brain injury combined with right femoral fractures in rats, a variety of serum biochemical indicators increase significantly, especially in early 3 days after injured. These indicators shows indirectly heart, liver and kidney organ dysfunction by trauma.

Animals ; Brain Injuries ; complications ; Femoral Fractures ; complications ; Male ; Multiple Organ Failure ; etiology ; metabolism ; pathology ; physiopathology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo examine the effect of icariin (ICA) on the cognitive impairment induced by traumatic brain injury (TBI) in mice and the underlying mechanisms related to changes in hippocampal acetylation level.

METHODSThe modifified free-fall method was used to establish the TBI mouse model. Mice with post-TBI cognitive impairment were randomly divided into 3 groups using the randomised block method (n=7): TBI (vehicle-treated), low-dose (75 mg/kg) and high-dose (150 mg/kg) of ICA groups. An additional sham-operated group (vehicle-treated) was employed. The vehicle or ICA was administrated by gavage for 28 consecutive days. The Morris water maze (MWM) test was conducted. Acetylcholine (ACh) content, mRNA and protein levels of choline acetyltransferase (ChAT), and protein levels of acetylated H3 (Ac-H3) and Ac-H4 were detected in the hippocampus.

RESULTSCompared with the sham-operated group, the MWM performance, hippocampal ACh content, mRNA and protein levels of ChAT, and protein levels of Ac-H3 and Ac-H4 were signifificantly decreased in the TBI group (P<0.05). High-dose of ICA signifificantly ameliorated the TBI-induced weak MWM performance, increased hippocampal ACh content, and mRNA and protein levels of ChAT, as well as Ac-H3 protein level compared with the TBI group (P<0.05).

CONCLUSIONICA improved post-TBI cognitive impairment in mice by enhancing hippocampal acetylation, which improved hippocampal cholinergic function and ultimately improved cognition.

Acetylation ; Acetylcholine ; metabolism ; Animals ; Brain Injuries, Traumatic ; complications ; Choline O-Acetyltransferase ; genetics ; metabolism ; Cognitive Dysfunction ; drug therapy ; etiology ; Flavonoids ; chemistry ; pharmacology ; therapeutic use ; Hippocampus ; pathology ; Histones ; metabolism ; Homeostasis ; drug effects ; Male ; Maze Learning ; drug effects ; Mice ; RNA, Messenger ; genetics ; metabolism

OBJECTIVETo investigate the relations between anti-myelin basic protein antibody (anti-MBP) variation and myelinoclasis in the brain stem following brain trauma.

METHODSIn rat models of brain trauma, MBP content and anti-MBP titer in the blood were measured using enzyme-linked immunosorbent assay (ELISA) at different time points after brain trauma, and the degree of myelinoclasis in the brain stem slices was assessed with osmic acid staining.

RESULTSEarly after brain trauma, MBP content in the blood increased followed by significant reduction 10 days later. Four days after the trauma, anti-MBP titer was markedly increased, accompanied by obvious exacerbation of myelinoclasis in the brain stem, both reaching the highest levels on day 10, at the point of which anti-MBP titer increased by 4 folds and the number of myelinoclasis by 10 folds compared with the control group. Anti-MBP titer and brain stem myelinolysis both lowered 30 days later. Correlation analysis showed an intimate positive correlation between anti-MBP titer and the degree of myelinoclasis.

CONCLUSIONAfter brain trauma, MBP is released as a specific antigen into the blood to stimulate the immune system for anti-MBP production, and the antibody is intimately related to the brain stem myelinoclasis.

Animals ; Antibodies ; metabolism ; Brain Injuries ; complications ; Brain Stem ; immunology ; pathology ; Demyelinating Autoimmune Diseases, CNS ; etiology ; immunology ; Female ; Male ; Myelin Basic Protein ; Nerve Tissue Proteins ; blood ; immunology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Transcription Factors ; blood ; immunology

To investigate the inhibiting effect of beta-Aescin on nuclear factor-kappaB (NF-kappaB) activation and the expression of tumor necrosis factor-alpha (TNF-alpha) protein after traumatic brain injury (TBI) in the rat brain, 62 SD rats were subjected to lateral cortical impact injury caused by a free-falling object and divided randomly into four groups: (1) sham operated (Group A); (2) injured (Group B); (3) beta-Aescin treatment (Group C); (4) pyrrolidine dithocarbamate (PDTC) treatment (Group D). Beta-Aescin was administered in Group C and PDTC treated in Group D immediately after injury. A series of brain samples were obtained directly 6 h, 24 h and 3 d respectively after trauma in four groups. NF-kappaB activation was examined by Electrophoretic Mobility Shift Assay (EMSA); the levels of TNF-alpha protein were measured by radio-immunoassay (RIA); the water content of rat brain was measured and pathomorphological observation was carried out. NF-kappaB activation, the levels of TNF-alpha protein and the water content of rat brain were significantly increased (P<0.01) following TBI in rats. Compared with Group B, NF-kappaB activation (P<0.01), the levels of TNF-alpha protein (P<0.01) and the water content of brain (P<0.05) began to decrease obviously after injury in Groups C and D. Beta-Aescin could dramatically inhibit NF-kappaB activation and the expression of TNF-alpha protein in the rat brain, alleviate rat brain edema, and that could partially be the molecular mechanism by which beta-Aescin attenuates traumatic brain edema.
Animals ; Body Water ; metabolism ; Brain Edema ; etiology ; metabolism ; pathology ; prevention & control ; Brain Injuries ; complications ; drug therapy ; metabolism ; pathology ; Escin ; administration & dosage ; NF-kappa B ; antagonists & inhibitors ; metabolism ; Pyrrolidines ; administration & dosage ; Rats ; Rats, Sprague-Dawley ; Thiocarbamates ; administration & dosage ; Treatment Outcome ; Tumor Necrosis Factor-alpha ; metabolism