To investigate the role of AQP9 in brain edema, the expression of AQP9 in an infectious rat brain edema model induced by the injection of lipopolysaccharide (LPS) was examined. Immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) analysis demonstrated that the expressions of AQP9 mRNA and protein at all observed intervals were significantly increased in LPS-treated animals in comparison with the control animals. Time-course analysis showed that the first signs of blood-brain barrier disruption and the increase of brain water content in LPS-treated animals were evident 6 h after LPS injection, with maximum value appearing at 12 h, which coincided with the expression profiles of AQP9 mRNA and protein in LPS-treated animals. The further correlation analysis revealed strong positive correlations among the brain water content, the disruption of the blood-brain barrier and the enhanced expressions of AQP9 mRNA and protein in LPS-treated animals. These results suggested that the regulation of AQP9 expression may play important roles in water movement and in brain metabolic homeostasis associated with the pathophysiology of brain edema induced by LPS injection.
Aquaporins/genetics ; Aquaporins/*metabolism ; Blood-Brain Barrier/metabolism ; Brain/drug effects ; Brain/physiology ; Brain Edema/chemically induced ; Brain Edema/*metabolism ; Lipopolysaccharides ; Rats, Sprague-Dawley ; Water/physiology

Administration, Oral ; Anti-Inflammatory Agents, Non-Steroidal ; adverse effects ; therapeutic use ; Aspirin ; adverse effects ; therapeutic use ; Brain Edema ; chemically induced ; Child ; Coma ; chemically induced ; Female ; Humans ; Liver ; drug effects ; pathology ; physiopathology ; Reye Syndrome ; chemically induced ; Treatment Outcome

Acupuncture Points ; Animals ; Brain ; pathology ; physiopathology ; Brain Edema ; etiology ; pathology ; physiopathology ; Cerebral Hemorrhage ; chemically induced ; pathology ; physiopathology ; Collagenases ; Electroacupuncture ; Heparin ; Male ; Rats ; Rats, Sprague-Dawley

To investigate the effects of triptolide on inflammation and apoptosis induced by focal cerebral ischemia/reperfusion in rats.The rat model of focal cerebral ischemia/reperfusion injury was established according to Longa's method. A total of 80 SD rats were randomly divided into 5 groups:normal control, sham group, DMSO group, middle cerebral artery occlusion (MCAO) group, and MCAO with tripolide treatment group. TTC staining was used to examine the site and volume of cerebral infarction, and Longa score was employed for neurological disorders measurement. Number of astrocytes was measured by fluorescence staining, and neuronal apoptosis was determined by TUNEL staining. The expressions of inducible nitric oxide synthase(iNOS), cyclooxygenase 2(COX-2) and NF-κB proteins were detected by immunohistochemistry, and the expression of iNOS, COX-2 mRNA was detected by real-time PCR.Compared with DMSO group and MCAO group, brain edema was improved (80.03±0.46)% (<0.05), infarct volume was reduced (8.3±1.4)% (<0.01), Longa score was decreased (1.38±0.20,<0.05) in triptolide treatment group. Meanwhile triptolide also dramatically reduced the number of GFAP-positive astrocytes (<0.05), alleviated protein expression of COX-2 (91.67±1.31), iNOS (95.24±5.07) and NF-κB (75.03±2.06) triggered by MCAO (all<0.05), and induced a down-regulation of cell apoptosis as showed by TUNEL assay (64.15±3.52,<0.05).Triptolide can reduce the cerebral infarction volume, attenuate brain edema and ameliorate the neurological deficits induced by cerebral ischemia-reperfusion injury rats, indicating that it might be used as a potential anti-inflammatory agent.
Animals ; Apoptosis ; drug effects ; Astrocytes ; Brain Edema ; drug therapy ; Brain Injuries ; chemically induced ; drug therapy ; Brain Ischemia ; chemically induced ; Cyclooxygenase 2 ; drug effects ; Diterpenes ; pharmacology ; Down-Regulation ; drug effects ; Epoxy Compounds ; pharmacology ; Infarction, Middle Cerebral Artery ; chemically induced ; drug therapy ; Inflammation ; drug therapy ; Male ; NF-kappa B ; drug effects ; Nitric Oxide Synthase Type II ; drug effects ; Phenanthrenes ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; chemically induced ; drug therapy

OBJECTIVETo investigate the effect of 1, 2-dichloroethane (1, 2-DCE) on blood brain barrier.

METHODSAcute toxic encephalopathy model was copied with the consecutive static inhalation of 1, 2-DCE. The water content of brain tissue was measured, and the blood brain barrier permeability was detected with lanthanum nitrate. The brain microvascular endothelial cells and neuroglial cells were cultured in vitro, which were administrated with 1, 2-DCE. The cell morphologic structures were observed under light microscope and electron microscope.

RESULTS(1) The extracellular edema was most found in the cerebral tissue and the leakage of lanthanum particles through the barrier were found with the lanthanum tracking method. (2) The water content in cerebral cortex in the moderate and high dose groups was significantly higher than that in the control group and became severer with the increases of the intoxicated time. The water content in cerebral medulla was significantly increased only at 6 hours after the intoxication. (3) The normal morphological structure of brain microvascular endothelial cells and neuroglial cells could be injured by 1, 2-DCE, and the injury to neuroglial cells caused by 1, 2-DCE occurred earlier and severer than that to brain microvascular endothelial cells.

CONCLUSION1, 2-DCE can damage blood brain barrier and induce cerebral edema.

Administration, Inhalation ; Animals ; Blood-Brain Barrier ; drug effects ; Brain ; pathology ; Brain Edema ; chemically induced ; pathology ; Cells, Cultured ; Dose-Response Relationship, Drug ; Endothelial Cells ; drug effects ; pathology ; Ethylene Dichlorides ; toxicity ; Female ; Male ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo observe the therapeutic effect of glucose-6-phosphate polyclonal antibody (G-6-P pAb) on vasogenic brain edema (VBE) in rats.

METHODSSixty Wistar rats were randomly divided into normal control group, VBE group, mannitol-treated edema group, and G-6-P pAb-treated edema group. After establishment of rat models of VBE by intraperitoneal injection of phenylephrine in the latter 3 groups, mannitol was injected through the femoral vein in mannitol group and G-6-P pAb injected intraperitoneally in G-6-P pAb group. The permeability of the blood-brain barrier (BBB) was determined by Evans blue (EB) extravasation method, and the brain water content in the gray and white matter measured with a moisture analyzer.

RESULTSG-6-P pAb administration significantly reduced the permeability of BBB as well as the water content in the white matter in comparison with mannitol treatment (P<0.01), but the two treatments showed no obvious difference in reducing the water content in the gray matter (P>0.05).

CONCLUSIONChanges in G-6-P activity results in BBB permeability alteration in the condition of VBE, and G-6-P pAb has a selective therapeutic effect against VBE, especially white matter edema.

Animals ; Antibodies, Monoclonal ; immunology ; therapeutic use ; Blood-Brain Barrier ; drug effects ; physiopathology ; Brain Edema ; chemically induced ; drug therapy ; physiopathology ; Capillary Permeability ; drug effects ; Female ; Glucose-6-Phosphate ; immunology ; Male ; Phenylephrine ; Random Allocation ; Rats ; Rats, Wistar

OBJECTIVEGlucocorticoid is considered as an effective drug for prevention and treatment of brain edema and reducing the blood-brain barrier (BBB) permeability. Intravenous immunoglobulin (IVIG) is frequently used to treat neurological diseases with immune abnormality, its function and potential mechanism on brain edema have not been reported. In this study, the roles of the total hydrosulfide group (TSH), non-protein hydrosulfide group (NPSH) and malondialdehyde (MDA) in etiology of the endotoxin brain edema in infant rats and the interfering effects of dexamethasone (DEX) and IVIG were investigated.

METHODSIn 35 infant rats, 10 mg/kg lipopolysaccharide (LPS) was intraperitoneally injected. The same volume of normal saline was injected to 24 control rats. Ten mg/kg DEX and 400 mg/kg IVIG were intravenously injected respectively to 36 and 24 infant rats instantly following LPS injection. The TSH, NPSH and MDA concentrations and the brain Evans blue contents were detected at different time in the brain tissue. The brain water content was measured by drying method.

RESULTSThe brain water, EB and MDA contents after endotoxin injection were significantly higher than those of control group, while the brain TSH, NPSH content were significantly lower than those of control group (P < 0.05 or P < 0.01); After treatment with DEX or IVIG, the brain EB, MDA and water content significantly decreased with the peak at 6 h (P < 0.05 or P < 0.01), TSH and NPSH significantly increased compared with LPS group. However, the NPSH content in IVIG treatment group did not change significantly (P > 0.05).

CONCLUSIONFree radicals play a role in the brain edema induced by LPS in infant rats. The primary results suggested that DEX and IVIG have therapeutic effect for the endotoxin-induced brain edema by affecting the free radicals.

Animals ; Blood-Brain Barrier ; drug effects ; metabolism ; Brain Edema ; chemically induced ; drug therapy ; metabolism ; Dexamethasone ; therapeutic use ; Endotoxins ; toxicity ; Free Radicals ; analysis ; Glucocorticoids ; therapeutic use ; Immunoglobulins, Intravenous ; administration & dosage ; therapeutic use ; Malondialdehyde ; analysis ; Rats ; Rats, Wistar ; Sulfides ; analysis

AIMTo determine the protective effect of ONO-1078, a leukotriene receptor antagonist, on focal cerebral ischemia induced by endothelin-1 in rats.

METHODSSlow microinjection of endothelin-1 (120 pmol in 6 microL, for > 6 min) into the region near the middle cerebral artery was used to induce focal cerebral ischemia. ONO-1078 (0.1 mg.kg-1) was i.p. injected 1 h before endothelin-1 injection. Neurological symptoms, brain edema, brain infarction size, and the survival neurons in cortex and striatum were observed 24 h after ischemia.

RESULTSIntracerebral microinjection of endothelin-1 induced remarkable neurological symptoms, brain infarction, brain edema, and decrease of survival neurons in the cortex and striatum. In rats pretreated with ONO-1078, endothelin-1-induced brain edema and brain infarction size were decreased. The numbers of survival neurons in striatum and cortex were increased significantly. The neurological symptoms were improved but not significantly.

CONCLUSIONONO-1078 possesses neuroprotective effect against cerebral ischemic injury induced by endothelin-1, therefore, leukotrienes may play a role in the injury of cerebral ischemia.

Animals ; Behavior, Animal ; drug effects ; Brain Edema ; pathology ; Brain Ischemia ; chemically induced ; pathology ; Cerebral Cortex ; pathology ; Cerebral Infarction ; pathology ; Chromones ; pharmacology ; Corpus Striatum ; pathology ; Endothelin-1 ; Leukotriene Antagonists ; pharmacology ; Male ; Neurons ; drug effects ; Neuroprotective Agents ; pharmacology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the effect of New Qingkailing injection (NQKLI) on cerebral edema following intracerebral hemorrhage (ICH) induced by collagenase VII in rats.

METHODSAfter being established into ICH model by collagenase VII, rats were treated with NQKLI by intraperitoneal injection. Forty-eight hrs later, brain contents of water was detected with wet and dry method, calcium content in brain was detected by atomic spectrophotometer, tumor necrosis factor-alpha (TNF-alpha) in brain tissue was determined by liquid competitive ibhibitory immunoassay, and serum matrix metalloproteinase-9 (MMP-9) were detected with enzyme-linked immunosorbent assay (ELISA) respectively.

RESULTSNQKLI reduced the contents of water, calcium and TNF-alpha content of brain tissue and serum MMP-9 in rats with ICH.

CONCLUSIONNQKLI could alleviate both vasogenic and cytotoxic cerebral edema by prohibiting calcium over-load, protecting basilar membrane and eliminating inflammation.

Animals ; Brain Edema ; etiology ; metabolism ; therapy ; Cerebral Hemorrhage ; chemically induced ; complications ; Collagenases ; Drugs, Chinese Herbal ; administration & dosage ; Injections ; Male ; Matrix Metalloproteinase 9 ; blood ; Neuroprotective Agents ; administration & dosage ; Phytotherapy ; Random Allocation ; Rats ; Rats, Wistar ; Tumor Necrosis Factor-alpha ; metabolism

The neuroprotective effect of propofol against intracerebral hemorrhage (ICH) in rats was investigated. ICH was induced in rats by infusion of collagenase (Type VII) 0.5 U (1 U x microL(-1)) into the left caudate nucleus. Three doses of propofol were given intraperitoneally (i.p.) 10 min before collagenase infusion. Effects of propofol on neurological behavioral scores, brain water content (BWC), activity of superoxide dismutase (SOD) and content of malondialdehyde (MDA) in brain tissue, expression level of caspase-3 were studied. In propofol groups (30 and 100 mg x kg(-1)), the neurological behavioral score, BWC and the content of MDA were significantly lower than those in ICH group (P < 0.05, P < 0.01), whereas the activity of SOD was higher than that in ICH group (P < 0.05). Meanwhile, propofol (15, 30, and 100 mg x kg(-1)) inhibited caspase-3 expression in dose-dependent manner (r = 0.877). Brain damages caused by ICH in rats can be alleviated by propofol, which mechanism might be attributed to its antioxidant activity.
Animals ; Behavior, Animal ; drug effects ; Brain ; metabolism ; Brain Edema ; drug therapy ; etiology ; Caspase 3 ; metabolism ; Cerebral Hemorrhage ; chemically induced ; complications ; metabolism ; physiopathology ; Collagenases ; Male ; Malondialdehyde ; metabolism ; Neuroprotective Agents ; pharmacology ; therapeutic use ; Propofol ; pharmacology ; therapeutic use ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; metabolism