Antioxidant action of a Chrysanthemum morifolium extract protects rat brain against ischemia and reperfusion injury.

The present study evaluated the potential neuroprotective effect and underlying mechanism of the total flavones extracted from Chrysanthemum morifolium (TFCM) against ischemia/reperfusion (I/R) injury. An animal model of cerebral ischemia was established by occluding the right middle cerebral artery for 90 minutes followed by reperfusion for 22 hours. The neurobehavioral scores, infarct area, and hemispheric edema were evaluated.

Bicyclol attenuates oxidative stress and neuronal damage following transient forebrain ischemia in mouse cortex and hippocampus.

To assess its potential neuroprotective effect against ischemia/reperfusion (IR) injury in mice, bicyclol was administered intragastrically once a day for 3 days. After 6h of bicyclol pretreatment on the third day, forebrain ischemia was induced for 1h by bilateral occlusion of the carotid arteries. After different times of reperfusion, the histopathological changes and the levels of mitochondria-generated reactive oxygen species (ROS), malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in the cortex and hippocampus were measured.

Genistein attenuates oxidative stress and neuronal damage following transient global cerebral ischemia in rat hippocampus.

Oxidative stress is believed to contribute to neuronal damage induced by cerebral ischemia/reperfusion (I/R) injury. The present study was undertaken to evaluate the possible antioxidant neuroprotective effect of genistein against neuronal death in hippocampal CA1 neurons following transient global cerebral ischemia in the rat. Transient global cerebral ischemia was induced in male Sprague-Dawley rats by four-vessel-occlusion for 10min.

Ischemic postconditioning protects against global cerebral ischemia/reperfusion-induced injury in rats.

Background And Purpose: Ischemic postconditioning has been found to decrease brain infarct area and spinal cord ischemic injury. In this study, we tested the hypothesis that ischemic postconditioning reduces global cerebral ischemia/reperfusion-induced structural and functional injury in rats.

Methods: Ten-minute global ischemia was induced by 4-vessel occlusion in male Sprague-Dawley rats.

Mitochondrial permeability transition dynamics: an indicator of mitochondrial potassium channel opener.

Mitochondrial permeability transition (MPT) is an intracellular event that is closely related to apoptosis and necrosis. However, whether this process underlies the recently reported neuroprotective potency of mitochondrial potassium channel openers applied in vivo remains uncertain. This study aims to clarify this issue by determining the effects of potassium channel openers on MPT dynamics in vitro along with their in vivo effects.

[Effect of activation of mitochondrial ATP sensitive potassium channel and calcium activated potassium channel on the permeability transition of mitochondria from both normal and ischemic rat brain].

Aim: To clarify whether the activation of mitochondrial ATP sensitive potassium channel and calcium activated potassium channel can influence the permeability transition of normal and ischemic brain mitochondria.

Methods: spectrophotometry was used to determine the effect of the two mitochondrial potassium channel agonists on the swelling of normal and ischemic brain mitochondria respectively.

Results: In normal mitochondria, diazoxide and NS1619 could inhibit the decrease of calcium induced mitochondrial absorbance at 520 nm (A520), which were blocked by atractyloside.

Reactive oxygen species mediate the neuroprotection conferred by a mitochondrial ATP-sensitive potassium channel opener during ischemia in the rat hippocampal slice.

Reactive oxygen species (ROS) are known to mediate the protection conferred by the opening of mitochondrial ATP-sensitive potassium channels (mitoK(ATP)) during ischemia in heart, but this has not been demonstrated in brain. The present study examined whether ROS mediate the neuroprotection conferred by a mitoK(ATP) opener during ischemia in rat hippocampal slices. Ischemia was simulated by oxygen and glucose deprivation.

[Changes in field excitatory postsynaptic potential and population spike in CA1 region of rat hippocampal slices following low-frequency stimulation].

The technique of extracellular recording was used and the changes in the slope of field excitatory postsynaptic potential (S-EPSP) and the amplitude of population spike (A-PS) were observed when homosynaptic long-term depression (LTD) was induced by low-frequency stimulation (LFS) in the CA1 region of rat hippocampal slices. After LFS of 900 pulses at 1 Hz was delivered, S-EPSP and A-PS were reduced by 35.4 +/- 5.

[Studies on properties of depotentiation of long-term potentiation induced by low frequency stimulation in CA1 neurons of rat hippocampal slices].

Aim And Methods: The parameters of low frequency stimulation (LFS) were altered systematically (frequencies of 1, 3 or 5 Hz; number of pulses of pulses of 300 or 900; and time lag after high frequency stimulation (HFS) of 20 or 100 min) and examined their effects on depotentiation (DP) of long-term potentiation (LTP) of synaptic transmission in CA1 neurons in hippocampal slices of rat.

Results: LTP could be induced by HFS (two trains of 100 Hz, 100 pulses, separated by 30 s) and be reversed to produce DP by a train of LFS of 900 pulses at 3 Hz given 20 min after HFS. DP induced by LFS could be blocked by NMDA receptor antagonist AP5 (50 micromol/L).