OBJECTIVES: This study was designed to investigate the neuroprotective effect of acupuncture in the middle cerebral artery occlusion-induced ischemia model. METHODS: Sprague-Dawley rats were randomly divided into two experimental groups: middle cerebral artery occlusion group (MCAO, n=8), and middle cerebral artery occlusion plus acupuncture group (MCAO + Acu, n=8). Acupuncture stimulation was given immediately after reperfusion. The effect of its stimulation to both GB34 and GB39 on the size of the brain infarct and the functional status of the brain cells after middle cerebral artery occlusion was examined by nissl staining and neuron-specific nuclear protein immunohistochemistry. RESULTS: The infarction volume was significantly decreased in the MCAO + Acu group (16.4 +/- 4.8%), compared with the MCAO group (39.9 +/- 10.2%). The number of neuron-specific nuclear protein-positive cells in the MCAO group was significantly decreased by 42.3 +/- 12.6% in the striatum and by 45.8 +/- 5.8% in the motor cortex, but the neuron-specific nuclear protein-positive cells in the MCAO + Acu group were rescued by 67.0 +/- 3.8% in the striatum and by 68.1 +/- 4.5% in the motor cortex, compared with the contralateral side (100%). DISCUSSION: This study showed that acupuncture had neuroprotective effects against focal ischemia in the middle cerebral artery occlusion model.

OBJECTIVES: This study was designed to investigate the neuroprotective effect of acupuncture in the middle cerebral artery occlusion-induced ischemia model. METHODS: Sprague-Dawley rats were randomly divided into two experimental groups: middle cerebral artery occlusion group (MCAO, n=8), and middle cerebral artery occlusion plus acupuncture group (MCAO + Acu, n=8). Acupuncture stimulation was given immediately after reperfusion. The effect of its stimulation to both GB34 and GB39 on the size of the brain infarct and the functional status of the brain cells after middle cerebral artery occlusion was examined by nissl staining and neuron-specific nuclear protein immunohistochemistry. RESULTS: The infarction volume was significantly decreased in the MCAO + Acu group (16.4 +/- 4.8%), compared with the MCAO group (39.9 +/- 10.2%). The number of neuron-specific nuclear protein-positive cells in the MCAO group was significantly decreased by 42.3 +/- 12.6% in the striatum and by 45.8 +/- 5.8% in the motor cortex, but the neuron-specific nuclear protein-positive cells in the MCAO + Acu group were rescued by 67.0 +/- 3.8% in the striatum and by 68.1 +/- 4.5% in the motor cortex, compared with the contralateral side (100%). DISCUSSION: This study showed that acupuncture had neuroprotective effects against focal ischemia in the middle cerebral artery occlusion model.

Turmeric has been in use since ancient times as a condiment and due to its medicinal properties. Curcumin, the yellow colouring principle in turmeric, is polyphenolic and major active constituent. Besides anti-inflammatory, thrombolytic and anticarcinogenic activities, curcumin also possesses strong antioxidant property. In view of the novel combination of properties, neuroprotective efficacy of curcumin was studied in rat middle cerebral artery occlusion (MCAO) model. Rats were subjected to 2 h of focal ischemia followed by 72 h of reperfusion. They were pre-treated with curcumin (100 mg/kg, po) for 5 days prior to MCAO and for another 3 days after MCAO. The parameters studied were behavioural, biochemical and histological. Treatment with curcumin could significantly improve neurobehavioral performance compared to untreated ischemic rats as judged by its effect on rota-rod performance and grid walking. A significant inhibition in lipid peroxidation and an increase in superoxide dismutase (SOD) activity in corpus striatum and cerebral cortex was observed following treatment with curcumin in MCAO rats as compared to MCAO group. Intracellular calcium levels were decreased following treatment with curcumin in MCAO rats. Histologically, a reduction in the infarct area from 33% to 24% was observed in MCAO rats treated with curcumin. The study demonstrates the protective efficacy of curcumin in rat MCAO model.

BACKGROUND AND PURPOSE:Low-level laser therapy (LLLT) modulates various biological processes. In the present study, we assessed the hypothesis that LLLT after induction of stroke may have a beneficial effect on ischemic brain tissue.

METHODS:Two sets of experiments were performed. Stroke was induced in rats by (1) permanent occlusion of the middle cerebral artery through a craniotomy or (2) insertion of a filament. After induction of stroke, a battery of neurological and functional tests (neurological score, adhesive removal) was performed. Four and 24 hours poststroke, a Ga-As diode laser was used transcranially to illuminate the hemisphere contralateral to the stroke at a power density of 7.5 mW/cm2.

RESULTS:In both models of stroke, LLLT significantly reduced neurological deficits when applied 24 hours poststroke. Application of the laser at 4 hours poststroke did not affect the neurological outcome of the stroke-induced rats as compared with controls. There was no statistically significant difference in the stroke lesion area between control and laser-irradiated rats. The number of newly formed neuronal cells, assessed by double immunoreactivity to bromodeoxyuridine and tubulin isotype III as well as migrating cells (doublecortin immunoactivity), was significantly elevated in the subventricular zone of the hemisphere ipsilateral to the induction of stroke when treated by LLLT.

CONCLUSIONS:Our data suggest that a noninvasive intervention of LLLT issued 24 hours after acute stroke may provide a significant functional benefit with an underlying mechanism possibly being induction of neurogenesis.

BACKGROUND AND PURPOSE:Low-level laser therapy (LLLT) modulates various biological processes. In the present study, we assessed the hypothesis that LLLT after induction of stroke may have a beneficial effect on ischemic brain tissue.

METHODS:Two sets of experiments were performed. Stroke was induced in rats by (1) permanent occlusion of the middle cerebral artery through a craniotomy or (2) insertion of a filament. After induction of stroke, a battery of neurological and functional tests (neurological score, adhesive removal) was performed. Four and 24 hours poststroke, a Ga-As diode laser was used transcranially to illuminate the hemisphere contralateral to the stroke at a power density of 7.5 mW/cm2.

RESULTS:In both models of stroke, LLLT significantly reduced neurological deficits when applied 24 hours poststroke. Application of the laser at 4 hours poststroke did not affect the neurological outcome of the stroke-induced rats as compared with controls. There was no statistically significant difference in the stroke lesion area between control and laser-irradiated rats. The number of newly formed neuronal cells, assessed by double immunoreactivity to bromodeoxyuridine and tubulin isotype III as well as migrating cells (doublecortin immunoactivity), was significantly elevated in the subventricular zone of the hemisphere ipsilateral to the induction of stroke when treated by LLLT.

CONCLUSIONS:Our data suggest that a noninvasive intervention of LLLT issued 24 hours after acute stroke may provide a significant functional benefit with an underlying mechanism possibly being induction of neurogenesis.

BACKGROUND:Inconsistent results have been reported for hyperbaric oxygen therapy (HBO) for acute stroke. We conducted a systematic review and meta-analysis to evaluate the benefit of HBO in animal studies of middle cerebral artery occlusion (MCAO).

METHODS:A systematic search of the literature published prior to September 2015 was performed using Embase, Medline (OvidSP), Web of Science and PubMed. Keywords included"hyperoxia"OR"hyperbaric oxygen"OR"HBO"AND"isch(a)emia"OR"focal cerebral ischemia"OR"stroke"OR"infarct"OR"middle cerebral artery occlusion (MCAO)."The primary endpoints were the infarct size and/or neurological outcome score evaluated after HBO treatment in MCAO. Heterogeneity was analyzed using Cochrane Library's RevMan 5.3.5.

RESULTS:Fifty-one studies that met the inclusion criteria were identified among the 1198 studies examined. When compared with control group data, HBO therapy resulted in infarct size reduction or improved neurological function (32% decrease in infarct size; 95% confidence interval (CI), range 28%-37%; p<0.00001). Mortality was 18.4% in the HBO group and 26.7% in the control group (RR 0.72, 95% CI, 0.54-0.98; p = 0.03). Subgroup analysis showed that a maximal neuro-protective effect was reached when HBO was administered immediately after MCAO with an absolute atmospheric pressure (ATA) of 2.0 (50% decrease; 95% CI, 43% -57% decrease; p<0.0001) and more than 6 hours HBO treatment (53% decrease; 95% CI, 41% -64% decrease; p = 0.0005).

CONCLUSIONS:HBO had a neuro-protective effect and improved survival in animal models of MCAO, especially in animals given more than 6 hours of HBO and when given immediately after MCAO with 2.0 ATA.