OBJECTIVETo investigate the early effect of thyrotropin-releasing hormone (TRH) on cerebral free radical reactions after acute brain injury in rabbits.

METHODS30 healthy white rabbits were randomly divided into three groups: Group A (n=10), Group B (n=12) and Group C (n=8). The rabbits in Group A and Group B were injured by direct hit. At 0.5-4 hours after injury, the rabbits in Group A were injected with TRH (8 mg/kg body weight) through a vein and the rabbits in Group B were injected with normal saline of equal volume. The rabbits in Group C served as the normal control. Then all the rabbits were killed and brain tissues were obtained. The content of lipoperoxide (LPO), the activity of superoxide dismutase (SOD) and the water content of the brain tissues were measured.

RESULTSThe contents of LPO and water in brain tissues in Group A were lower and the activity of SOD was higher than those of Group B (P<0.05). After injury, intracranial pressure (ICP) rose rapidly and continuously with time passing by. When TRH was given to the animals in Group A, the rising speed of ICP slowed down significantly.

CONCLUSIONSTRH can decrease the cerebral free radical reactions and cerebral edema after acute brain injury in rats.

Animals ; Brain Edema ; etiology ; prevention & control ; Brain Injuries ; complications ; metabolism ; Female ; Free Radicals ; metabolism ; Intracranial Pressure ; Lipid Peroxidation ; Male ; Rabbits ; Superoxide Dismutase ; metabolism ; Thyrotropin-Releasing Hormone ; pharmacology

OBJECTIVETo observe the effects of ganglioside GM1 on reduction of brain edema and amelioration of cerebral metabolism after traumatic brain injury (TBI).

METHODSAn acute experimental closed TBI model in rats was induced by a fluid-percussion brain injury model. At five and sixty minutes after TBI, the animals were intraperitoneally injected by ganglioside GM1 (30 mg/kg) or the same volume of saline. At the 6th hour after TBI, effects of ganglioside GM1 or saline on changes of mean arterial pressure (MAP), contents of water, lactic acid (LA) and lipid peroxidation (LPO) in the injured cerebral tissues were observed.

RESULTSAfter TBI, MAP decreased and contents of water, LA and LPO increased in brain injury group; however, MAP was back to normal levels and contents of water, LA and LPO decreased in ganglioside GM1 treated group, compared with those in brain injury group (P < 0.05). No significant difference between the saline treated group and the brain injury group (P > 0.05) was observed.

CONCLUSIONSGanglioside GM1 does have obvious neuroprotective effect on early TBI.

Animals ; Brain ; metabolism ; Brain Edema ; etiology ; prevention & control ; Brain Injuries ; complications ; metabolism ; Disease Models, Animal ; Hexosyltransferases ; therapeutic use ; Lactic Acid ; analysis ; Lipid Peroxidation ; Male ; Random Allocation ; Rats ; Rats, Sprague-Dawley

The goal of this study was to introduce a new method inducing an experimental brain injury model using ESWL(Extracorporeal Shock Wave Lithotripsy) and to evaluate findings of localized lesions on 1H MR imaging and the response of cerebral energy metabolism using a 31P MR spectroscope to the ESWL brain injury in cats. This study also examined effects of cerebral protective drugs. 1) There were no statistically significant changes in pH at all measurement points. 2) In the trauma group, initial decrease of PCr/Pi was seen at 30 to 60 minutes with return to control levels by 2 hours after injury(P < 0.05), followed by a second decline at 4 hours which lasted until 8 hours after injury. 3) Significant recovery in PCr/Pi(P < 0.05) was observed in both the THAM and dexamethasone treated groups at all measurement points and in the mannitol treated group only temporary recovery at 30 and 60 minutes (P < 0.05). 4) High intensity signals were seen on 1H MR imaging in traumatized animals. This study demonstrated the immediate and persistent recovery of cerebral energy metabolism using THAM or dexamethasone and an immediate but transient effect with mannitol in traumatized animals.
Adenosine Triphosphate/metabolism ; Animals ; Brain/*drug effects/metabolism ; Brain Injuries/etiology/metabolism/*prevention & control ; Cats ; Dexamethasone/*therapeutic use ; *Disease Models, Animal ; Energy Metabolism/*drug effects ; Hydrogen-Ion Concentration ; *Lithotripsy ; Magnetic Resonance Spectroscopy ; Phosphates/metabolism ; Phosphocreatine/metabolism ; Random Allocation ; Tromethamine/*therapeutic use

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