PURPOSE: This study was done to identify whether pre-conditioning exercise has neuroprotective effects against cerebral ischemia, through enhance brain microvascular integrity. METHODS: Adult male Sprague-Dawley rats were randomly divided into four groups: 1) Normal (n=10); 2) Exercise (n=10); 3) Middle cerebral artery occlusion (MCAo), n=10); 4) Exercise+MCAo (n=10). Both exercise groups ran on a treadmill at a speed of 15 m/min, 30 min/day for 4 weeks, then, MCAo was performed for 90 min. Brain infarction was measured by Nissl staining. Examination of the remaining neuronal cell after MCAo, and microvascular protein expression on the motor cortex, showed the expression of Neuronal Nuclei (NeuN), Vascular endothelial growth factor (VEGF) & laminin. RESULTS: After 48 hr of MCAo, the infarct volume was significantly reduced in the Ex+MCAo group (15.6+/-2.7%) compared to the MCAo group (44.9+/-3.8%) (p<.05), and many neuronal cells were detected in the Ex+MCAo group (70.8+/-3.9%) compared to the MCAo group (43.4+/-5.1%) (p<.05). The immunoreactivity of laminin, as a marker of microvessels and Vascular endothelial growth factor (VEGF) were intensively increased in the Ex+MCAo group compared to the MCAo group. CONCLUSION: These findings suggest that the neuroprotective effects of exercise pre-conditioning reduce ischemic brain injury through strengthening the microvascular integrity after cerebral ischemia.
Animals ; Brain Infarction/pathology ; Disease Models, Animal ; Infarction, Middle Cerebral Artery/metabolism/pathology/*prevention & control ; Laminin/metabolism ; Male ; Microvessels/metabolism ; Neurons/metabolism ; *Physical Conditioning, Animal ; Rats ; Rats, Sprague-Dawley ; Stroke/prevention & control ; Vascular Endothelial Growth Factor A/metabolism

OBJECTIVETo investigate the protective effect of leptin against cerebral ischemia/reperfusion injury in mice.

METHODSMouse models of transient focal cerebral ischemia were established by occlusion of the right middle cerebral artery for 2 h followed by 24 h reperfusion. The infarct volume and neurological deficit scores following leptin treatment were determined using TTC staining and the Longa's score, respectively, to evaluate the protective effect of leptin against ischemic cerebral injury. The levels of lactate dehydrogenase (LDH), malondialdehyde (MDA) and nitric oxide (NO) in the brain tissue were measured by colorimetry. The histopathological changes in the brain were observed with HE staining, and the expression of glial fibrillary acidicprotein (GFAP) was detected by immunohistochemistry.

RESULTSLeptin treatment markedly reduced cerebral infarct volume and neurological deficits induced by transient ischemia. The LDH, MDA and NO levels in the brain tissues were significantly decreased after leptin treatment, which also alleviated the histopathological injury, maintained the normal morphology of the astrocytes and increased the expression of GFAP.

CONCLUSIONLeptin produces obvious protective effect against cerebral ischemia/reperfusion injury by inhibiting lipid peroxidation, stabilizing the internal environment and adjusting the activity of the astrocytes.

Animals ; Brain ; drug effects ; pathology ; Brain Ischemia ; Infarction, Middle Cerebral Artery ; metabolism ; pathology ; L-Lactate Dehydrogenase ; metabolism ; Leptin ; pharmacology ; Male ; Malondialdehyde ; metabolism ; Mice ; Nitric Oxide ; metabolism ; Reperfusion Injury ; metabolism ; pathology ; prevention & control ; Time Factors

OBJECTIVETo observe the effect of cyclovirobuxinum-D (CVB-D) on cerebral ischemia-reperfusion injury in rats and explore its mechanisms.

METHODOne hundred and twenty rats were randomly divided into three CVB-D groups (2, 1, 0.5 mg x kg(-1)), Nimodipine group (2 mg x kg(-1)), model group and sham operated group, 20 rats each group. Rat cerebral ischemia-reperfusion injury model was induced by middle cerebral artery occlusion, the nerve injury symptoms was evaluated, the level of SOD and MDA in brain tissue were determined, the concentration of intracellar Ca2+ of brain was measured, and the pathological change of brain was also observed.

RESULTCVB-D could improve the nerve injury symptoms, reduce the infarction area of brain, the concentration of intracellar Ca2+ and the level of MDA, increase the activity of SOD, and decrease the pathological change of brain.

CONCLUSIONCVB-D has protective effect on cerebral ischemia-reperfusion injury in rats.

Animals ; Brain ; drug effects ; metabolism ; pathology ; Buxus ; chemistry ; Calcium ; metabolism ; Drugs, Chinese Herbal ; isolation & purification ; pharmacology ; Infarction, Middle Cerebral Artery ; complications ; Male ; Malondialdehyde ; metabolism ; Neuroprotective Agents ; isolation & purification ; pharmacology ; Plants, Medicinal ; chemistry ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; etiology ; metabolism ; prevention & control ; Superoxide Dismutase ; metabolism

OBJECTIVETo investigate the effects of caffeic acid ester fraction (Caf) from Erigeron breviscapus, mainly composed of dicaffeoylquinic acids (diCQAs), on microglial activation in vitro and focal cerebral ischemia in vivo.

METHODSThe production of nitric oxide (NO), tumor necrosis factor α (TNF-α), and interleukin-1β (IL-1β) induced by lipopolysaccharide (LPS) treatment in rat primary cultured microglia were measured by Griess reaction or enzyme-linked immunosorbent assay. Cell viability of cortical neurons was measured using AlamarBlue reagent. The behavioral tests and the infarct area of brain were used to evaluate the damage to central nervous system in rat middle cerebral artery occlusion (MCAO) model of cerebral ischemia. Real time polymerase chain reaction was used to determine the expression of inducible nitric oxide synthase (iNOS), TNF-α and IL-1β mRNA in ischemic cerebral tissues.

RESULTSCaf inhibited the production of NO, TNF-α and IL-1β induced by LPS treatment in primary microglia in a dose-dependent manner. Exposure of cortical neurons to conditioned medium from Caf-treated microglia increased neuronal cell viability (P<0.01) compared with conditioned medium from LPS-treated alone. In MCAO rat model of cerebral ischemia, Caf could significantly improve neurobehavioural performance and reduce percentage infarct volume compared with the vehicle group (P<0.05). Caf could also significantly inhibit the up-regulation of iNOS, TNF-α, and IL-1β gene expressions in ischemic cerebral tissues.

CONCLUSIONCaf could suppress microglial activation, which may be one mechanism of its neuroprotective effect against ischemia.

Animals ; Brain ; drug effects ; metabolism ; pathology ; Brain Ischemia ; complications ; drug therapy ; pathology ; prevention & control ; Caffeic Acids ; chemistry ; pharmacology ; Chemical Fractionation ; Chromatography, High Pressure Liquid ; Erigeron ; chemistry ; Gene Expression Regulation ; drug effects ; Infarction, Middle Cerebral Artery ; complications ; pathology ; Interleukin-1beta ; genetics ; metabolism ; Microglia ; drug effects ; metabolism ; pathology ; Neuroprotective Agents ; chemistry ; pharmacology ; therapeutic use ; Nitric Oxide Synthase Type II ; genetics ; metabolism ; Plant Extracts ; pharmacology ; Quinic Acid ; analogs & derivatives ; chemistry ; pharmacology ; therapeutic use ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Wistar ; Tumor Necrosis Factor-alpha ; genetics ; metabolism

OBJECTIVETo investigate the protective effects of resveratrol on inflammatory process induced by focal cerebral ischemia-reperfusion in rats.

METHODRats were pretreated with resvreratrol at the dose of 10, 20, 40 mg kg(-1) for 7 days and then subjected to cerebral ischemia/reperfusion induced by a middle cerebral artery occlusion (MCAO). The infarct volume and the neurological deficit were determined by the method of TTC (2, 3, 5-triphenylterazolium chloride) staining and Longa's score. The permeability of blood-brain barrier (BBB) was evaluated by measurement of the evans blue (EB) content in the brain with spectrophotometer. The content of interleukin-lbeta, interleukin-6 (IL-6, IL-1beta) in serum and tumor necrosis factor-alpha (TNF-alpha), myeloperoxidase (MPO) in brain were determined by radio-immunoassay and ELISA assay.

RESULTResveratrol reduced infarct volume, ameliorated the neurological deficit and the permeability of BBB, the content of IL-6, IL-1beta in serum and TNF-alpha, MPO activity in brain tissue also were significantly decreased.

CONCLUSIONThese results showed that resveratrol had protective effects on cerebral injury by inhibiting the releasing of the inflammatory mediators after ischemia/reperfusion injury.

Animals ; Blood-Brain Barrier ; drug effects ; Brain ; drug effects ; metabolism ; pathology ; Brain Ischemia ; complications ; Infarction, Middle Cerebral Artery ; blood ; etiology ; prevention & control ; Inflammation Mediators ; blood ; Interleukin-1beta ; blood ; Interleukin-6 ; blood ; Male ; Neuroprotective Agents ; pharmacology ; Peroxidase ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; complications ; Stilbenes ; pharmacology ; Tumor Necrosis Factor-alpha ; metabolism