ABSTRACT
Aim To investigate the effect of 13-methyl- tetradecanoic acid (13-MTD) on brain edema after cerebral ischemia in rats and its mechanism. Methods The model of middle cerebral artery occlusion (MCAO) was prepared by suture embolization method. Thirty minutes prior to the insertion of the embolus, tail vein injection of 13-MTD 40, 80, 120 nig • kg"1 (M40, M80, M120) was respectively performed. The negative control group was given an equal volume of liposomes. 6, 12 and 24 h after ischemia, neurological deficits were observed with Ixmga neurological deficit scores; brain infarct volume was observed with TTC staining; brain edema was calculated with AutoCAD image analysis software; brain water content was measured with brain dry weight; the blood-brain barrier (KB). AQP4 mRNA expression in the injured brain tissue was detected by KT-PCR. The expression of AQP4 protein in the injured brain tissues was detected by immunohistochemistry. Results 13-MTD could significantly improve the symptoms of neurological deficits in rats with cerebral ischemia, reduce the volume of cerebral infarction, decrease brain water content and cerebral edema, and down-regulate EB leakage, and up-regulate the expression of AQP4 in the ischemic brain tissues. Conclusion 13-MTD can reduce brain edema after cerebral ischemia in rats by regulating AQP4 expression.
ABSTRACT
This study was designed to detect the impact of Valerian Ligusticum Pill (VLP) on cerebral ischemia reperfusion injury in rats, and explore the mechanism of angiogenesis. Sixty SD male rats were randomly divided into five groups, including sham operation group, model group, VLP-low (30mg·kg-1) group, VLP-high (50mg·kg-1) group and nimodipine (10mg·kg-1) group. The ischemia reperfusion injury model was induced by occlusion of middle cerebral artery with suture embolus, reperfusion after 30 minutes' ischemia. When the rats were awake, the first neurological function scores was determined with modified neurological severity score (mNSS). The rats were given VLP (30mg·kg-1, 50mg·kg-1) and nimodipine (10mg·kg-1) through intragastric administration at 2 mL, once a day for a total of 7 days, while an equal amount of distilled water was used in the sham operation group and model control group. After 7 days, the rats were given second neurological function scores, and improvement of neurological function=[the first score]-[the second score]. The rats were sacrificed to investigate the infarction volume percentage with 2,3,5-triphenyl tetrazolium chloride method; do the qualitative and half quantitative analyses for protein vascular endothelial growth factor receptor 2 (VEGFR2) in the tissue of cortex infarction around by Western blot; detect the new blood vessels of cortex infarction around by ki67/lectin immunofluorescence double staining method. Results suggest that VLP could significantly improve the neurological function, reduce the percentage of infarct volume, increase the expression of VEGFR2 and number of new blood vessels in the cortex infarction around compared with model group. In conclusion, VLP may relive the acute cerebral ischemia reperfusion injury in rats by inducing angiogenesis.
ABSTRACT
[Abstract ] Objective The spleen plays an important role in brain ischemia-induced cerebral injury.This study aimed to ex-plore the correlation of the spleen mass index with the neurological function scores and infarction volume following permanent occlusion of the middle cerebral artery ( pMCAO) in rats. Methods Thirty male SD rats were equally randomized into a sham operation, a 3-day brain ischemia, and a 7-day brain ischemia group.The pMCAO model was established by ligation in the right brain of the rats. Neurological function scores were obtained with the Longa 5-Point Scale at 0, 3, and 7 days after modeling, and at 3 and 7 days, the spleen mass index was calculated, the infarction volume measured by TTC, and brain histopathological changes evaluated by HE stai-ning. Results Compared with the 7-day ischemia group, the 3-day ischemia rats showed significantly reduced spleen mass index ([1.62 ±0.58] vs [0.87 ±0.59] mg/g) and increased neurological function score (1.00 [1.00, 1.25] vs 2.00 [1.75, 2.25]) and infarct volume ([18.67 ±7.92] vs [36.20 ±14.92]%) (all P<0.05).An extremely significant decrease was found in the spleen mass index of the 3-day ischemia rats in comparison with that of the animals in the sham operation group ([1.90 ±0.22] mg/g) (P<0.01).HE staining revealed more obvious pathological injury of the cerebral cortex in the 3-day than in the 7-day group.The spleen mass index was negatively correlated with the neurological dys-function score (r=-0.851, P=0.019) and infarction volume (r=-0.717, P =0.013). Conclusion In pMCAO rats, measure-ment of the spleen mass index contributes significantly to the preven-tion and improvement of ischemia-induced cerebral injury.
ABSTRACT
OBJECTIVE: To investigate the protective effect of the decoction of tartary buckwheat flavonoids on focal cerebral is-chemia-reperfusion injury of rats. MEHTODS: Fifty male SD rats will be randomly divided into normal group, cerebral ischemia-reperfusion group (model group), high dose of tartary buckwheat flavonoids group, middle dose of tartary buckwheat flavonoids group and low dose of tartary buckwheat flavonoids group, each groups of 10 rats. A rat model of the right middle cerebral artery occlusion/reper-fusion(MCAO) was established by the filament method. After being operated, treatment-group rats will be administered 100,75 and 50 mg · kg-1 of the decoction of tartary buckwheat flavonoids three times a day for 7 consecutive days, after administrated for 7 d, rats in each group will undergo neurobehavioral tests. Expressions of cerebral inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) were measured by SP immunohistochemistry. The optical density value (OD) was measured by imaging analysis, and the percentage of cells with iNOS and eNOS positive expression was analyzed under light microscope. RESULTS: Compared with ischemia-reperfusion group, neurological function score increased in the decoction of tartary buckwheat flavonoids groups. Treatment groups had lower expression level of iNOS but higher expression level of eNOS than those in the model groups (P < 0.01, P < 0.05). The number of neurons of Hippocampal CA1 was increased (P < 0.05). CONCLUSION: Tartary buckwheat flavonoids can improve neurological function and decrease the expression of iNOS and increase the expression of eNOS in cerebral ischemia-reperfusion rats, which may contribute to the protection of neural function.