• Journal of Acupuncture Research
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• v.24 no.2
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• pp.125-140
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• 2007

Objectives: This study was performed to investigate the effects of acupuncture therapy(AT, AT-9), electro-acupuncture therapy(EAT) and low level laser acupuncture therapy(LAT) at LRJ on the focal ischemia-induced by intraluminal filament insertion in rats. Methods : In the present syudy, the focal ischemia was induced by Intraluminal filament insertion into left middle cerebral artery. The subjects were divided into five groups after focal brain ischemia. (n=15, in each group) : Control with no treatment, AT with acupuncture at $LR_3$, AT-9 with acupuncture at $LR_3$ and rotating 9 times in a clockwise direction, EAT with electro-acupuncture at $LR_3$ and LAT with invasive laser acupuncture at $LR_3$. Anti-apoptotic and neuroprotective effects of acupuncture were observed by mGluR5 mRNA, Bax mRNA, Bcl-2 mRNA, Cytochrome C protein, Cresyl violet-stain and Choline acetyltransferase (ChAT)-stain in the hippocampus. Results: 1. In LAT, mGluR5, Cresyl violet-stain and ChAT-stain were increased. 2. In LAT, Cytochrome C protein was decreased. 3. In AT-9, Bax, Cytochrome C protein and the Bax/Bcl-2 ratio were decreased. 4. In AT-9, Bcl-2, Cresyl violet-stain and ChAT-stain were increased. 5. In EAT, Bcl-2 and Cresyl violet-stain were increased. Conclusions: These results suggests that LAT and AT-9 show anti-apoptotic and neuro-protective effects and that LAT and AT-9 may be useful for managing stroke by focal brain ischemia.

• Biomedical Science Letters
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• v.15 no.1
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• pp.17-23
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• 2009

The prevalence of patent foramen ovale (PFO) in healthy persons was estimated as about $10{\sim}25%$ and was up to 40% in patients with stroke. Transesophageal echocardiography (TEE) was considered to be the most sensitive method to detect PFO and was used as the gold standard. Transcranial doppler sonography (TCD) of the middle cerebral artery (MCA) during a contrast (saline bubble) injection has recently been proposed as an alternative detecting method for PFO. In this study, we would like to know the difference between TCD value and TEE value in subjects with cryptogenic ischemic stroke. We performed TCD and TEE tests to detect PFO on 64 patients (30 women and 34 men, mean age was 59.4 years) with cryptogenic ischemic stroke. PFO prevalence through TCD was 45.3% (29 of 64 patients) and the prevalence through TEE was 34.4% (22 of 64 patients). There was no statistical significance between PFO test and TCD test (P=0.206). But TCD had a sensitivity of 90.9% (20 of 22 patients), specificity of 78.6% (33 of 42 patients), positive predictive value of 69.0% (20 of 29 patients), and negative predictive value of 94.3% (33 of 35 patients). We concluded that TCD was a highly sensitive method for detecting a right-left shunt. Therefore, the non-invasive TCD test is a method more effective than the anti-invasive TEE test in the cost and evaluation of the existence or nonexistence of right to left shunt in addition to the screening method of the cerebrovascular disorder. Considering these points, TCD test could be recommended for patients with cryptogenic ischemic stroke as a useful and convenient method for screening of the existence or nonexistence of a right to left shunt caused by PFO.

• The Korean Journal of Physiology and Pharmacology
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• v.12 no.5
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• pp.275-280
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• 2008

A brief ischemic insult induces significant protection against subsequent massive ischemic events. The molecular mechanisms known as preconditioning (PC)-induced ischemic tolerance are not completely understood. We investigated whether kinetic changes of cyclooxygenase (COX)-2 during reperfusion time-periods after PC were related to ischemic tolerance. Rats were given PC by occlusion of middle cerebral artery (MCAO) for 10 min and sacrificed after the indicated time-periods of reperfusion (1, 2, 4, 8, 12, 18 or 24 h). In PC-treated rats, focal ischemia was induced by occlusion of MCA for 24 h and brain infarct volume was then studied to determine whether different reperfusion time influenced the damage. We report that the most significant protection against focal ischemia was obtained in rats with 8 h reperfusion after PC. Administration of indomethacin (10 mg/kg, oral) or rofecoxib (5 mg/kg, oral) 48 h prior to PC counteracted the effect of PC. Immunohistochemical analysis showed that COX-2 and HO-l protein were induced in PC-treated rat brain, which was significantly inhibited by rofecoxib. Taken together, we concluded that the kinetic changes of COX-2 expression during the reperfusion period after PC might be partly responsible for ischemic tolerance.

• Journal of Korean Neurosurgical Society
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• v.30 no.sup2
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• pp.316-321
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• 2001

Objectives : The goal of this study is to evaluate the usefulness of mild hypothermia treatment in patients with increased intracranial pressure(ICP). Material and Method : From November 1999 to May 2001, 11 patients were treated with mild hypothermia ($32-34^{\circ}C$) in whom ICP maintained at higher than 20mmHg in spite of decompressive surgery and high dose barbiturate therapy. The patient's rectal temperature were lowered by external cooling. Hypothermia was maintained for not more than 7 days and then the patients were rewarmed slowly for 24 hours. If increased ICP persisted for 2 days of hypothermia, this treatment was continued for several days. The functional outcome of each patient was assessed according to Glasgow Outcome Scale(GOS). Results : All cases except two cases showed decrease of ICP after hypothermia therapy. In 1 case which was right middle cerebral artery(MCA) infarct, ICP re-increased after 24 hours and in another 1 case, ICP was not controlled initially. Among 11 cases, 3 cases showed favorable outcome. Conclusion : Mild hypothermia treatment in patients with increased ICP was effective in controlling ICP and mortality was so decreased. More clinical experience and controlled study was need to determine the effectiveness.

• Molecules and Cells
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• v.45 no.4
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• pp.216-230
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• 2022

SERTA domain-containing protein 1 (Sertad1) is upregulated in the models of DNA damage and Alzheimer's disease, contributing to neuronal death. However, the role and mechanism of Sertad1 in ischemic/hypoxic neurological injury remain unclear. In the present study, our results showed that the expression of Sertad1 was upregulated in a mouse middle cerebral artery occlusion and reperfusion model and in HT22 cells after oxygen-glucose deprivation/reoxygenation (OGD/R). Sertad1 knockdown significantly ameliorated ischemia-induced brain infarct volume, neurological deficits and neuronal apoptosis. In addition, it significantly ameliorated the OGD/R-induced inhibition of cell viability and apoptotic cell death in HT22 cells. Sertad1 knockdown significantly inhibited the ischemic/hypoxic-induced expression of p-Rb, B-Myb, and Bim in vivo and in vitro. However, Sertad1 overexpression significantly exacerbated the OGD/R-induced inhibition of cell viability and apoptotic cell death and p-Rb, B-Myb, and Bim expression in HT22 cells. In further studies, we demonstrated that Sertad1 directly binds to CDK4 and the CDK4 inhibitor ON123300 restores the effects of Sertad1 overexpression on OGD/R-induced apoptotic cell death and p-Rb, B-Myb, and Bim expression in HT22 cells. These results suggested that Sertad1 contributed to ischemic/hypoxic neurological injury by activating the CDK4/p-Rb pathway.

• Journal of Ginseng Research
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• v.47 no.2
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• pp.274-282
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• 2023

Background: Ginsenoside compound K (CK) stimulated activation of the PI3K-Akt signaling is one of the major mechanisms in promoting cell survival after stroke. However, the underlying mediators remain poorly understood. This study aimed to explore the docking protein of ginsenoside CK mediating the neuroprotective effects. Materials and methods: Molecular docking, surface plasmon resonance, and cellular thermal shift assay were performed to explore ginsenoside CK interacting proteins. Neuroscreen-1 cells and middle cerebral artery occlusion (MCAO) model in rats were utilized as in-vitro and in-vivo models. Results: Ginsenoside CK interacted with recombinant human PTP1B protein and impaired its tyrosine phosphatase activity. Pathway and process enrichment analysis confirmed the involvement of PTP1B and its interacting proteins in PI3K-Akt signaling pathway. PTP1B overexpression reduced the tyrosine phosphorylation of insulin receptor substrate 1 (IRS1) after oxygen-glucose deprivation/reoxygenation (OGD/R) in neuroscreen-1 cells. These regulations were confirmed in the ipsilateral ischemic hemisphere of the rat brains after MCAO/R. Ginsenoside CK treatment reversed these alterations and attenuated neuronal apoptosis. Conclusion: Ginsenoside CK binds to PTP1B with a high affinity and inhibits PTP1B-mediated IRS1 tyrosine dephosphorylation. This novel mechanism helps explain the role of ginsenoside CK in activating the neuronal protective PI3K-Akt signaling pathway after ischemia-reperfusion injury.

• Journal of the Korean Society of Radiology
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• v.17 no.6
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• pp.809-817
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• 2023

Single source and dual source measurements using anthropomorphic phantoms in which the phantoms are lined up in human body equivalents use OSLD (Optically Stimulated Luminescence Dosimeter), so the effective dose is calculated using OSLD. For hospital images, SNR (Signal to Noise Ratio) and CNR (Contrast to Noise Ratio) were measured in MCA (Middle Cerebral Artery) for single source and dual source, and for phantom images, SNR and CNR were measured for brain parenchyma of single source and dual source. For hospital imaging, SNR and CNR were measured in MCA for both single-source and dual-source, and for phantom images, SNR and CNR were measured for brain parenchyma from single-source and dual-source. As a result of comparing the SNR and CNR of the hospital image and the phantom image, there was no statistical difference. Comparing patient doses in hospital images, the effective dose of the dual source was 53.53% less and the effective dose of the dual energy phantom was 57.94% less. The dose can be increased in other areas, but the cerebrovascular area is useful because the dose is small.

• Journal of Pharmacopuncture
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• v.27 no.2
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• pp.162-171
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• 2024

Objectives: Electroacupuncture (EA) has been demonstrated to aid stroke recovery. However, few investigations have focused on identifying the potent molecular targets of EA by comparing EA stimulation between naïve and disease models. Therefore, this study was undertaken to identify the potent molecular therapeutic mechanisms underlying EA stimulation in ischemic stroke through a comparison of mRNA sequencing data obtained from EA-treated naïve control and ischemic stroke mouse models. Methods: Using both naïve control and middle cerebral artery occlusion (MCAO) mouse models, EA stimulation was administered at two acupoints, Baihui (GV20) and Dazhui (GV14), at a frequency of 2 Hz. Comprehensive assessments were conducted, including behavioral evaluations, RNA sequencing to identify differentially expressed genes (DEGs), functional enrichment analysis, protein-protein interaction (PPI) network analysis, and quantitative real-time PCR. Results: EA stimulation ameliorated the ischemic insult-induced motor dysfunction in mice with ischemic stroke. Comparative analysis between control vs. MCAO, control vs. control + EA, and MCAO vs. MCAO + EA revealed 4,407, 101, and 82 DEGs, respectively. Of these, 30, 7, and 1 were common across the respective groups. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses revealed upregulated DEGs associated with the regulation of inflammatory immune response in the MCAO vs. MCAO + EA comparison. Conversely, downregulated DEGs in the control vs. control + EA comparison were linked to neuronal development. PPI analysis revealed major clustering related to the regulation of cytokines, such as Cxcl9, Pcp2, Ccl11, and Cxcl13, in the common DEGs of MCAO vs. MCAO + EA, with Esp8l1 identified as the only common downregulated DEG in both EA-treated naïve and ischemic models. Conclusion: These findings underscore the diverse potent mechanisms of EA stimulation between naïve and ischemic stroke mice, albeit with few overlaps. However, the potent mechanisms underlying EA treatment in ischemic stroke models were associated with the regulation of inflammatory processes involving cytokines.

• Journal of Life Science
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• v.19 no.11
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• pp.1658-1665
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• 2009

This study was carried out on thirty men to define the association of inflammatory markers with physiological factors on one-time aerobic exercise (for 15 min. Post-exercise interleukin-6 (IL-6), mean corpuscular hemoglobin concentration (MCHC), heart rate (HR), systolic blood pressure (SBP), and pulsatility and resistance index of middle cerebral artery (PI and RI, respectively) levels were elevated compared to those measured pre-exercise. Total leukocyte and platelet counts, high-sensitivity C-reactive protein (hs-CRP), free radical (FR), and low density lipoprotein cholesterol (LDL) levels tended to decrease after exercise. Pre-exercise IL-6 levels were positively correlated with pre-exercise SBP levels, while post-exercise IL-6 level was positively correlated with post-exercise PI and RI levels. Post-exercise, hs-CRP levels were negatively related to SBP and HR. Pre-exercise, FR levels were positively associated to SBP, DBP, and HR. Post-exercise FR levels were negatively related to the post-exercise blood flow velocity in middle cerebral artery. Pre-exercise erythrocyte indices (RBC, MCV, MCH, and MCHC levels) were in inverse proportion to pre-exercise IL-6 levels. Post-exercise FR levels were inversely related to post-exercise total leukocyte, lymphocyte, monocyte, and MCH levels. Pre-exercise $Mg^{++}$ levels were in inverse proportion to pre-exercise IL-6, hs-CRP, or FR levels. These findings suggest that one-time aerobic exercise offers a significant relationship between inflammatory markers and some biochemical markers or electrolytes. Further studies need to be carried out for investigation of differences between genders or age groups following one-time or regular aerobic exercise.

• The Korea Journal of Herbology
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• v.23 no.2
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• pp.159-168
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• 2008

Objectives : The present study has been undertaken to investigate the effects of Dipsaci Radix on Muscle Fiber Atrophy and MyoD Expression in Gastrocnemius of MCAO Rats Methods : In order to investigate effects of Dipsaci radix on the skeletal muscle atrophy following stroke, cerebral infarct was induced by the middle cerebral artery occlusion (MCAO) in the rats. Water extract of Dipsaci radix (184.4 mg/100 g) was treated for 4 weeks, once a day orally, after the MCAO. Effects were evaluated with muscle fiber type composition and cross-sectioned area of muscle fibers in gastrocnemius of the unaffected & affected hind limbs. And MyoD protein expression in gastrocnemius was demonstrated with immunohistochemistry and western blotting. Results : Obtained results were as follows; 1. Infarct volume was not attenuated by Dipsaci radix treatment in the MCAO rats. 2. At the affected-side hind limb of the MCAO rats, the increase of type-I fibers and the decrease of type-II fibers were induced by Dipsaci radix treatment. 3. At the affected-side hind limb of the MCAO rats, decreases of cross-sectioned areas of type-I and type-II fibers were attenuated by Dipsaci radix treatment. 4. At the affected-side hind limb of the MCAO rats, MyoD positive cells were increased by Dipsaci radix treatment. 5. At the affected-side hind limb of the MCAO rats, MyoD expressions were increased by Dipsaci radix treatment. Conclusions : These results suggest that Dipsaci radix has a protective effect against muscle atrophy, through the inhibition of the muscle cell apoptosis, following the central nervous system demage.