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Protective effects of Ginkgo biloba extract on rats during cerebral ischemia/reperfusion
Bo Hu1, Shenggang Sun, Guangwu Mei
1Neurology Department, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. hubo@hust.edu.cn
Objective:
To study the effect of Ginkgo biloba extract on rats during ischemia/reperfusion and its influence on intracellular calcium in hippocampal neurons.
Methods:
Model of intraluminal occlusion of the middle cerebral artery (MCAO) was used to prepare the ischemia/reperfusion cortex tissue. Concentration of MDA was determined by measuring thiobarbituric acid-reactive substance. GSH-PX was quantified using the thiobarbituric acid (TBA) technique. SOD was assayed througha xanthine method. Endogenous amino acids were quantified by high performance liquid chromatographic (HPLC) analysis. Primary culturs of hippocampal neurons were prepared for a free intracellular calcium ([Ca(2+)]I) assay by Fura-2 based single cell microfluoremetric technique.
Results:
Comparing control and treatment groups, the concentration of SOD and GSH-PX were higher, whereas that of MDA was much lower; the concentration of glutamate and aspartate decreased and that of GABA increased markedly at all time point (P < 0.01), Gly also decreased at some time points (P < 0.05). The differences were significant between the groups of 10 mg/kg, 15 mg/kg and the groups of 5 mg/kg. When 1 x 10(-5) mol/L glutamate was applied with 25 micro g/ml ginkgo biloba extract to cultured neurons, the increase in [Ca(2+)]I was lower than that caused by applying glutamate alone. Its peak value was much lower and increased phase was longer, its declining phase was shorter. After returning to baseline, the application of 1 x 10(-5) mol/L glutamate could induce the reaction to recover.
Conclusions:
Ginkgo biloba extract could protect damaged neurons by keeping the balance of inhibitory/excitatory aminoacids, enhancing the free radical scavengers system, and inhibiting the effect of glutamate on [Ca(2+)]I.
Insights
Ginkgo biloba extract protects brain cells from damage during stroke by balancing neurotransmitters and reducing oxidative stress. It also inhibits glutamate's harmful effect on intracellular calcium levels in neurons.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Ischemia/reperfusion injury significantly impacts brain tissue, leading to neuronal damage.
- Intracellular calcium ([Ca(2+)]I) dysregulation is a key mechanism in excitotoxicity during stroke.
- Ginkgo biloba extract is investigated for its potential neuroprotective properties.
Purpose of the Study:
- To evaluate the neuroprotective effects of Ginkgo biloba extract in a rat model of cerebral ischemia/reperfusion.
- To determine the influence of Ginkgo biloba extract on intracellular calcium levels in hippocampal neurons.
Main Methods:
- Middle cerebral artery occlusion (MCAO) model for inducing ischemia/reperfusion in rats.
- Biochemical assays for oxidative stress markers: malondialdehyde (MDA), glutathione peroxidase (GSH-PX), and superoxide dismutase (SOD).
- High-performance liquid chromatography (HPLC) for quantifying amino acids and Fura-2 microfluorimetry for intracellular calcium ([Ca(2+)]I) in cultured hippocampal neurons.
Main Results:
- Ginkgo biloba extract treatment increased SOD and GSH-PX levels while decreasing MDA concentration, indicating reduced oxidative stress.
- Significant alterations in amino acid levels were observed, with decreased glutamate and aspartate and increased GABA.
- In cultured neurons, Ginkgo biloba extract attenuated glutamate-induced increases in intracellular calcium ([Ca(2+)]I).
Conclusions:
- Ginkgo biloba extract demonstrates neuroprotective effects against ischemia/reperfusion injury.
- The extract helps maintain the balance between excitatory and inhibitory amino acids.
- It enhances the endogenous free radical scavenging system and modulates glutamate-induced calcium influx.