Hyun Duk Yang

Neuroprotective Activity of Triterpenoid Saponins from Platycodi radix Against Glutamate-induced Toxicity in Primary Cultured Rat Cortical Cells

During our investigation of the neuroprotective activity of Platycodi radix we found that an aqueous extract of this folk medicine exhibited significant protection against glutamate-induced toxicity in primary cultured rat cortical cells. In order to clarify the neuroprotective mechanism(s) of this observed effect, activity-guided isolation was performed to seek and identify active fractions and components. By such fractionation, four known triterpene saponin compounds--platycodins A, C and D and deapioplatycodin D--were isolated from the n-butanol fraction. Among these four compounds, platycodin A exhibited significant neuroprotective activities against glutamate-induced toxicity, exhibiting cell viability of about 50%, at concentrations ranging from 0.1 microM to 10 microM. Therefore, the neuroprotective effect of Platycodi radix might be due to the inhibition of glutamate-induced toxicity by the saponin compounds it contains.

Bis(4-hydroxybenzyl)sulfide: a Sulfur Compound Inhibitor of Histone Deacetylase Isolated from Root Extract of Pleuropterus ciliinervis

A sulfur compound, bis(4-hydroxybenzyl)sulfide (1) was isolated from the root extract of Pleuropterus ciliinervis. Its structure was elucidated using NMR spectroscopic techniques and mass spectrometric analysis. Compound 1 showed potent inhibitory activity in a histone deacetylase (HDAC) enzyme assay. It also exhibited growth inhibitory activity on five human tumor cell lines and more sensitive inhibitory activity on the MDA-MB-231 breast tumor cell line.

Facilitation and reciprocal inhibition by imagining thumb abduction

It is well known that motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) of the motor cortex are facilitated by voluntary muscle contraction. We evaluated the effects of imagination of movements on MEP latencies of agonist and antagonist muscles in the hand using TMS. Twenty-two healthy volunteers were studied. TMS delivered at rest and while imagining tonic abduction of the right thumb. MEPs were recorded in response to magnetic stimulation over the scalp and cervical spine (C7-T1), and central motor conduction times (CMCT) were calculated. MEPs were recorded from right abductor pollicis brevis muscle (APB) and adductor pollicis muscle (AP) simultaneously. Imagination of abduction resulted in a shortened latency of MEPs in the APB muscle, and a prolonged latency in the AP muscle. But the imagination caused no significant change in the latency of MEPs elicited by stimulation over the cervical spine. The changes of the CMCT may account for these latency changes with imagination of movement. These findings indicate that imagination of thumb abduction facilitates motoneurons of agonist muscle and has an inhibitory effect on those of antagonist muscle (reciprocal inhibition).

Recovery of reversed basilar artery flow as seen by transcranial sonography and MRA source images for vertebral dissection.

The dissection of the intracranial vertebral artery (VAD) is a common cause of young age brain stem stroke. VAD can be detected by conventional angiography, but there is yet no agreement on the most effective tool to use for the detection of VAD. Here, we report a patient with VAD, who was diagnosed with an intimal flap within the left vertebral artery by the magnetic resonance angiography (MRA) source images. Transcranial Doppler (TCD) showed a reversed flow in the basilar artery. After 4 months, TCD and transcranial color‐coded Doppler (TCCD) confirmed a normal anterograde flow of the vertebro‐basilar arteries.

Medullary Hemorrhage after Ischemic Wallenberg's Syndrome in a Patient with Cavernous Angioma

Background The main complication of cerebral cavernous angioma is hemorrhage. Ischemic stroke as a complication of cerebral cavernous angioma has rarely been described, and hemorrhage after ischemic Wallenbergs syndrome has not been reported before. Case Report A 45-year-old woman presented with perioral numbness, hoarseness, dysphagia, and worsening of her previous sensory symptoms. The patient had been taking aspirin for 3 years after suffering from ischemic Wallenbergs syndrome with left paresthesia as a residual symptom. Brain computed tomography revealed an acute medullary hematoma in the previously infarcted area. Follow-up magnetic resonance imaging revealed a cavernous angioma in the right medulla. Conclusions We presume that cerebral cavernous angioma was responsible for both the ischemia and the hemorrhage, and we also cautiously speculate that the aspirin contributed to the development of hemorrhage in the previously infarcted area.

Inhibition of β-amyloid1-40 Peptide Aggregation and Neurotoxicity by Citrate

The accumulation of beta-amyloid (Abeta) aggregates is a characteristic of Alzheimers disease (AD). Furthermore, these aggregates have neurotoxic effects on cells, and thus, molecules that inhibit Abeta aggregate formation could be valuable therapeutics for AD. It is well known that aggregation of Abeta depends on its hydrophobicity, and thus, in order to increase the hydrophilicity of Abeta, we considered using citrate, an anionic surfactant with three carboxylic acid groups. We hypothesized that citrate could reduce hydrophobicity and increase hydrophilicity of Abeta(1-40) molecules via hydrophilic/electrostatic interactions. We found that citrate significantly inhibited Abeta(1-40) aggregation and significantly protected SH-SY5Y cell line against Abeta(1-40) aggregates-induced neurotoxicity. In details, we examined the effects of citrate on Abeta(1-40) aggregation and on Abeta(1-40) aggregates-induced cytotoxicity, cell viability, and apoptosis. Th-T assays showed that citrate significantly inhibited Abeta(1-40) aggregation in a concentration-dependent manner (Th-T intensity: from 91.3% in 0.01 mM citrate to 82.1% in 1.0 mM citrate vs. 100.0% in Abeta(1-40) alone). In cytotoxicity and viability assays, citrate reduced the toxicity of Abeta(1-40) in a concentration-dependent manner, in which the cytotoxicity decreased from 107.5 to 102.3% as compared with Abeta(1-40) aggregates alone treated cells (127.3%) and the cell viability increased from 84.6 to 93.8% as compared with the Abeta(1-40) aggregates alone treated cells (65.3%). Furthermore, Hoechst 33342 staining showed that citrate (1.0 mM) suppressed Abeta(1-40) aggregates-induced apoptosis in the cells. This study suggests that citrate can inhibit Abeta(1-40) aggregation and protect neurons from the apoptotic effects of Abeta(1-40) aggregates. Accordingly, our findings suggest that citrate administration should be viewed as a novel neuroprotective strategy for AD.