| Background and Purpose: Ginkgo biloba extract (GBE) can play a role in reducing brain damage.From various experiments in vivo and in vitro, it is concluded that GBE hasneuroprotective properties. PAF antagonism, free-radical and NOscavenging, synaptic plasticity and excitability and interaction withneurotransmitters are possible mechanisms of action. In focal cerebralischemia there are some profound cellular and molecular changes whichinvolve upregulation of inflammatory cytokines, activation of microgliaand so on. Microglia can be activated during cerebral ischemia and damageas one of responsive cells of inflammation and immunity in central nervoussystem. But it was not clear whether or not GBE can affect theinflammation response in brain ischemia as a possible neuroprotectivemechanism. We adopted focal cerebral ischemia model by photothrombosisin mice, and used Movement Capture Analysis( MoCA) to accuratelyrecord instantaneous locomotion and evaluate neurological injury in miceafter various treatments. To observe the neuroprotective effects of GBE inthis model, and the corresponding expression of CD11b on the surface ofmicroglia. We want to know whether and how GBE can possibly regulatethe responses of CD11b-IR positive cell and to explore an mechanism ofGBE neuroprotection in cerebral ischemia. Materials and Methods: 150 adult Balb/c mice were randomized to divided into sixgroups:(1)Control group(n=25). (2) Illumination 30min group(n=25).(3) Rose Begnal B ( n=25 ) . (4)Ischemia group ( n=25 ) . (5)GBEpretreatment group ( n=25 ) . (6) Dexamethasone treatment group(n=25), as a positive control. GBE pretreated with intraperitoneallydoses of 100mg/kg/day. On the 7th day, mice were anaesthetized and focalcerebral ischemia was induced. Injection of the photosensitive dye Rosebengal B via vena caudalis, subsequent focal illumination of the brain witha cold light source through the intact skull led to focal cortical infarct.Animals were sacrificed at 0.5h, 6h, 1d, 3d, 7d respectively afterphotothrombosis and infarction volume was determined by 2,3,5-triphenyltetrazolium chloride (TTC), Hematoxylin and eosin(HE) and Nisslstaining showed the histological change. Microglia response assessed byimmunohistochemistry against CD11b. Results: 1. MoCA: We compared Mean±SD of the difference of average heihtin bilateral forelimbs. It has a significant difference between the ischemiagroup and the control group (P<0.001). Compared to the ischemia group,GBE pretreatment group and dexamethasone treatment group can decreasethe difference of average heiht in bilateral forelimbs. however, There is nosignificant difference between the later two groups. 2. TTC: The infarction volume was showed by Mean±SD. Asignificant reduce of the infarction volume was found in the GBEpretreatment group and dexamethasone treatment group compare toischemia group(P<0.01). but there was no significant difference betweenGBE pretreatment group and dexamethasone treatment group. 3. Histopathology: 3.1. HE: Cell lost in the lesion core, and some anachromasis cellsapperanced. 3.2. Nissl staining: The number of neuron in ischemia group notablydecreased than control group in the lesion periphery(P<0.001). Comparedto ischemia group, the number of neuron increased in GBE pretreatmentgroup and Dexamethasone treatment group, the number of neuron in thelater two groups is similar. 3.3. CD11b-immunoreactivity(CD11b-IR): In the lesion peripherydifferent stages of CD11b-IR positive cells activation accompanied withthe increasing of ischemia damage. GBE pretreatment significantly reducedthe number(P<0.001)and increased the main gray of CD11b-IR positivecells (P<0.001)in the lesion periphery of ischemia, and the potency ofinhibition is similar to the dexamethasone pretreatment group. Conclusion: 1. A photochemical induced cerebral focal ischemia model of the miceis a well-characterized model. The neuroprotective effects of severalcompounds have been tested using this model. It has many advantages,such as reproducible size, location and geometry. 2. MoC...
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