• The Journal of Korean Medicine
• /
• v.26 no.1 s.61
• /
• pp.174-186
• /
• 2005

Objectives : The water extract of Samul-tang (SMT) has traditionally been used for treatment of ischemic heart and brain damage in oriental medicine. However, little is known about the mechanism by which the water extract of SMT rescues cells from these damages. Methods: This study was designed to investigate the protective mechanisms of SMT on oxidative stress-induced toxicity in H9c2 cardiomyoblast cells. Treatment with $H_2O_2$ markedly induced death of H9c2 cardiomyoblast cells in a dose-dependent manner. Results: The characteristics of H20z-induced death of H9c2 showed apparent apoptotic features such as DNA fragmentation and morphological change. However, SMT significantly reduced both H202-induced cell death and morphological change. The decrease of Bc-2 expression by High were inhibited by SMT. In addition, the increase of Bax expression was also inhibited by SMT. The cotreatment of SMT and $H_2O_2$ in H9c2 cells also induced the phosphorylation of ERK in a time-dependent manner. Moreover, PD98059, a specific inhibitor of ERK1/2 attenuated the protective effects of SMT on $H_2O_2-induced$ toxicity in H9c2 cardiomyoblast cells. These results suggest that both ERK1/2 signaling pathways play important roles in the protective effects of SMT on $H_2O_2-induced$ apoptotic death of H9c2 cells. Also, the expression profile of proteins in $H_2O_2$ cardiomyoblast cells were screened by using two-dimensional (2-D) gel electrophoresis. Among 300 spots resolved in 2-D gels, the comparison of control versus apoptosis cells revealed that signal intensity of 17 spots increased and 11 spots decreased. Conclusions: Taken together, this study suggests that the protectiw effects of the water extract of SMT against oxidative damages may be mediated by the modulation of Bc1-2 and Bax expression via the regulation of the ERK signaling pathway.

• Journal of Haehwa Medicine
• /
• v.9 no.1
• /
• pp.745-761
• /
• 2000

Literatural study for Delirious speech and Fading murmuring, the results were as follows. 1. Delirious speech and Fading murmuring are given at the speech impediment. Derious speech to be out of language's order and slur the end of his words, and Fading murmuring is to repeat in losing conscious. 2. In constrast with Delirious speech and Fading murmuring, Maniac speech is induced by a general term for manic-depressive psychosis. Luoyan is to say in a feeble voice and mumble in a sleeping condition, and Paraphasia and Solioquy are appeared in a clear mental condition. The speech impediment is caused by damages of the nervous system and speech organ, and Yuyancuoluan is appeared in a feverless condition. 3. The symptoms of Delirious speech are to utter ravings and have a loud and heavy voice, and these resemble the delirium which specially has a speech impediment and muddle in the western medical world. The symptoms of Fading murmuring are to speak ambigously, repeatedly, and illogically and so are similar to the Wernicke dysphasia which is caused by a incomprehensible conversation. 4. The causes of Delirious speech are to spread a stomach heat and the lungs pathogenic qi into heart, not to sweat in cold damage, the Three Yang Combination of syndrome, stomach repletion, yang collapse due to excessive sweat, diarrhea, after diarrhea, heat to enter the blood chamer, feces to remain in the stomach, stasis blood to enter the viscera, to carry anger to extremity, and to be constipated. the cause of Fading murmuring is to despair vacuity desertion of vital essence and energy after a serious illness. 5. The causes of delirium are general infection, postoperative states, and metabolism disorders and those of Wernicke dysphasia are disorders of the blood vessel, brain tumors and traumas. 6. Delirious speech is cured with the discrimination of vacuity and repletion. Baitong Tang(白通湯), Chaihu Guizhi Tang(柴胡桂枝湯), Chaihu Jia Longgu Muli Tang(柴胡加龍骨牡蠣湯) are prescribed in case of vacuity, while Chengqi Tang(承氣湯), Baihu Tang(白虎湯), Liangge San(凉膈散) are in case of repletion. Fading murmuring is treated with Xiao Chaihu Tang(小柴胡湯), Fuzi Tang Jiawei(附子湯加味), Shengmai San(生脈散), and Renshen Sanbai Tang(人蔘三白湯). 7. To acupunture Qimen-Xue(期門穴) is required when it is late to prescribe a medical decoction or the hyperactive liver qi attacking the spleen.

• Journal of Acupuncture Research
• /
• v.22 no.2
• /
• pp.1-12
• /
• 2005

Objective: With the onset of stroke, white blood cells release several proinflammatory cytokines, including interleukin (IL)-6, IL-10, and tumor necrosis factor $(TNF)-{\alpha}$. It has been proven in previous studies that the release of these cytokines is related to the extent of damage to the brain and to overall prognosis. However, no studies have yet been performed to determine the connection with IL-6 and IL-10. Thus, this study is performed to see whether polymorphisms of IL-6, IL-10, and $TNF-{\alpha}$ genes that show increased serum concentration with the onset of stroke are related to stroke attack in Koreans. Methods : Peripheral blood samples derived from patients with stroke (n=100) and healthy controls (n=100) were taken under informed consent. In subjects with stroke, blood samples were obtained within 24 hours of stroke onset. Genomic DNA was isolated using the Wizard DNA Purification Kit (Promega, Madison, WI). Results : 1. Subjects with Heterozygote (GA) and Homozygote (AA) $TNF-{\alpha}$ gene types showed 2.433 and 20.457 times higher risks of being attacked by stroke, respectively, compared to subjects with wild type (GG) $TNF-{\alpha}$ gene type. The data was still statistically significant after adjusting for age, sex, history of smoking, and history of alcohol drinking. 2. Subjects with Homozygote (CC) IL-6 gene type showed 182.033 times higher risk of being attacked by stroke, compared to subjects with wild type (GG) IL-6 genes. This data was statistically insignificant (p=0.700). The data was still statistically insignificant after adjusting for age, sex, history of smoking, and history of alcohol drinking. 3. Subjects with Heterozygote (GA) and Homozygote (GG) IL-10 gene types showed 8.785 and 3.303 times higher risks of being attacked by stroke, respectively, compared to subjects with wild type (AA) IL-10 genes. The data was still statistically insignificant after adjusting for age, sex, history of smoking, and history of alcohol drinking. Conclusion : Our results suggest that the investigated $TNF-{\alpha}$ and IL-10 gene polymorphisms play an important role in stroke attack, but IL-6 gene polymorphism has not been found to associated with stroke.

• Journal of dental hygiene science
• /
• v.10 no.5
• /
• pp.341-347
• /
• 2010

This paper reports is a descriptive study for analyzing the knowledge level and educational condition of dental hygiene students regarding cardiopulmonary resuscitation(CPR). This study was implemented from May 24, 2010 to June 4, 2010. The results were as follows: 1. The score was low for the knowledge level of CPR (3.72 out of 8.0). 2. The knowledge level of CPR was higher in the students with heart disease in their family than in those without(t=5.725, P<0.05). 3. While students had a high percentage of correct answers e.g. 93.5% and 73.8% for the mouth-to-mouth CPR and hand position in pressing the upper part of the belly, they had low percentage of correct answers, e.g. 8.2%, 28.9%, 25.4%, and 49.2% for consciousness and breathing check, maintaining the airway and the time to brain damage from a heart attack, respectively. 4. The students used TV(55.2%) and the Internet(20.1%) as the medium for observing CPR. 5. 60.2% of students did not have any training in CPR. 6. More than 90.0% of students required training in CPR. Most of the students requested CPR training when they attended middle and high school. They had hoped to receive CPR training at school or a specialized training organization. In conclusion, the knowledge level of CPR of dental hygiene students is low, and the need for training and participation is high. Therefore, dental hygiene students should receive CPR training.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.21 no.4
• /
• pp.891-897
• /
• 2007

This experimental Study was designed to investigate the mechanism of Acanthopanacis Cortex Roots(ACR) 50% ethyl alcohol extract on the improvement of regional cerebral blood flow and cytokines production in cerebral ischemic rats. And was designed to investigate whether ACR inhibits lactate dehydrogenase(LDH) activity in neuronal cells The results were as follows; ACR significantly inhibited LDH activity in neuronal cells. These results suggest that ACR prevents the neuronal death. rCBF was significantly and stably increased by ACR(10 mg/kg, i.p.) during the period of cerebral reperfusion, which contrasted with the findings of rapid and marked increase in control group. In cytokine production of serum by drawing from femoral arterial blood at 1 hr after middle cerebral arterial occlusion, experimental group was significantly decreased $IL-1{\beta}$ and $TNF-{\alpha}$ production, and significantly increased IL-10 production compared with control group. In cytokine production of serum by drawing from femoral arterial blood at 1 hr after reperfusion, experimental group was significantly decreased $IL-1{\beta}$ and $TNF-{\alpha}$ production, and significantly increased IL-10 production compared with control group. According to above results, the author suggest that ACR had an anti-ischemic effect through the improvement of cerebral hemodynamics, and inhibitive effect on the brain damage by inhibited $IL-1{\beta}$ and $TNF-{\alpha}$ production, and accelerated IL-10 production.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.17 no.4
• /
• pp.1082-1091
• /
• 2003

To elucidate the neuroprotective effect of Kamijihwang-hwan(KSH) on nerve cells damaged by hypoxia, the cytotoxic effects of exposure to hypoxia were determined by XTT, NR, MTT and SRB asssay. The activity of catalase and SOD was measured by spectrophometry, and TNF-α and PKC activity was measured after exposure to hypoxia and treatment of Kamijihwang-hwan(KSH) water extract(KJHWE). Also the neuroprotective effect of KJHWE was researched for the elucidation of neuroprotective mechanism. The results were as follows ; Hypoxia decreased cell viability measured by XTT, NR assay when cultured cerebral neurons were exposed to 95% N2/5% CO₂ for 2～26 minutes in these cultures and KJHWE inhibited the decrease of cell viability. H₂O₂ treatment decreased cell viability measured by MTT, and SRB assay when cultured cerebral neurons were exposed to 1-80 uM for 6 hours, but KJHWE inhibited the decrease of cell viability. Hypoxia decreased catalase and SOD activity, and also TNF-α and PKC activity in these cultured cerebral neurons, but KJHWE inhibited the decrease of the catalase and SOD activity in these cultures. Hypoxia triggered the apoptosis via caspase activation and internucleosomal DNA fragmentation. Also hypoxia stimulate the release of cytochrome c form mitochondria. KJHWE inhibited the apoptosis via caspase activation induced by hypoxia. From these results, it can be suggested that brain ischemia model induced hypoxia showed neurotoxity on cultured mouse cerebral neurons, and the KJHWE has the neuroprotective effect in blocking the neurotoxity induced by hypoxia in cultured mouse cerebral neurons.

• Molecules and Cells
• /
• v.37 no.3
• /
• pp.226-233
• /
• 2014

Excessive reactive oxygen species (ROS) generated from abnormal cellular process lead to various human diseases such as inflammation, ischemia, and Parkinson's disease (PD). Sensitive to apoptosis gene (SAG), a RING-FINGER protein, has anti-apoptotic activity and anti-oxidant activity. In this study, we investigate whether Tat-SAG, fused with a Tat domain, could protect SH-SY5Y neuroblastoma cells against 1-methyl-4-phenylpyridinium ($MPP^+$) and dopaminergic (DA) neurons in the substantia nigra (SN) against 1-methyl-4-phenyl-1,2,3,6-tetra-hydropyridine (MPTP) toxicity. Western blot and immunohistochemical analysis showed that, unlike SAG, Tat-SAG transduced efficiently into SH-SY5Y cells and into the brain, respectively. Tat-SAG remarkably suppressed ROS generation, DNA damage, and the progression of apoptosis, caused by $MPP^+$ in SH-SY5Y cells. Also, immunohistochemical data using a tyrosine hydroxylase antibody and cresyl violet staining demonstrated that Tat-SAG obviously protected DA neurons in the SN against MPTP toxicity in a PD mouse model. Tat-SAG-treated mice showed significant enhanced motor activities, compared to SAG- or Tat-treated mice. Therefore, our results suggest that Tat-SAG has potential as a therapeutic agent against ROS-related diseases such as PD.

• Journal of Korean Neurosurgical Society
• /
• v.30 no.sup2
• /
• pp.294-299
• /
• 2001

Objectives : CT-guided stereotactic evacuation for spontaneous intracerebral hemorrhage can minimize the brain damage and can be performed safely and simply under local anesthesia. But that procedure is time consuming and has a risk of rebleeding because of the stress during head pin fixation. So authors describe easy and precise guidelines for FHA of putaminal hemorrhage without stereotactic instrument. Methods and Materials : We analyzed the data of 298 patients who underwent CT-guided stereotactic aspiration of putaminal hematoma in our hospital between January 1990 and December 2000. We divided the patients into three groups according to the location of hematoma : anterior portion, middle portion and posterior portion of putamen. Total number of catheters inserted into the hematoma were 345 and there were with regard to the direction and depth of catheters. Results : Proposed guidelines of catheter insertion to putaminal hemorrhage in our institution. 1) hematoma at the anterior portion of putamen ; Direction of catheter was the midpupillary line of the eye and the point intersecting a line drawn from the burr hole to a point between external auditory meatus(EOM) and 1cm posterior to EOM. Depth of catheter was 6-6.5cm. 2) hematoma at the middle portion of putamen ; Direction of catheter was the midpupillary line of the the eye and the point intersecting a line drawn from the burr hole to a point between 1cm and 2cm posterior to EOM. Depth of catheter was 6.5-7cm. 3) hematoma at the posterior portion of putamen ; Direction of catheter was 15 degree laterally from the midpupillary line of the eye and the point intersecting a line drawn from the burr hole to a point between 2cm and 3cm posterior to EOM. Depth of catheter was 7-7.5cm. We have performed FHA of putaminal hemorrhage in 48 cases according to this guideline. All catheter were inserted exactly at the center of hematoma and average operation time was about 30 minutes. Conclusion : Our proposed guidelines for putaminal hemorrhage are considered to be safe and simple method with similar accuracy and rapid decompression compared with traditional stereotactic method. Main advantages of this technique were unnecessity of stereotactic frame application and less time requirement for hematoma removal.

• Journal of The Korean Ophthalmological Society
• /
• v.59 no.11
• /
• pp.1097-1102
• /
• 2018

Purpose: To report a case of toxic optic neuropathy caused by chlorfenapyr ingestion accompanied by central nervous system involvement. Case summary: A 44-year-old female visited our clinic complaining of reduced visual acuity in both eyes for 7 days. She had ingested a mouthful of chlorfenapyr for a suicide attempt 2 weeks prior to the visit. Gastric lavage was performed immediately after ingestion at the other hospital. Her best-corrected visual acuity was finger count 30 cm in the right eye and hand motion in the left eye. Both pupils were dilated by 5.0 mm and the response to light was sluggish in both eyes. A relative afferent pupillary defect was detected in her left eye. Funduscopy revealed optic disc swelling in both eyes. Magnetic resonance imaging of the brain showed a symmetric hyper-intense signal in the white matter tract including the internal capsule, corpus callosum, middle cerebellar peduncle, and brainstem. The patient was diagnosed with toxic optic neuropathy induced by chlorfenapyr ingestion, and underwent high-dose intravenous corticosteroid pulse therapy. Three days later, the best-corrected visual acuity was no light perception in both eyes. Three months later, optic atrophy was observed in both eyes. Optical coherence tomography revealed a reduction in the thicknesses of the retinal nerve fiber layer and ganglion cell and inner plexiform layer in the macular area. Conclusions: Ingestion of even a small amount of chlorfenapyr can cause severe optic nerve damage through the latent period, despite prompt lavage and high-dose steroid treatment.

• Journal of Life Science
• /
• v.31 no.2
• /
• pp.237-247
• /
• 2021

Immune responses in the central nervous system (CNS) function as the host's defense system against pathogens and usually help with repair and regeneration. However, chronic and exaggerated neuroinflammation is detrimental and may create neuronal damage in many cases. The NOD-, LRR-, and pyrin domain―containing 3 (NLRP3) inflammasome, a kind of NOD-like receptor, is a cytosolic multiprotein complex that consists of sensors (NLRP3), adaptors (apoptosis-associated speck like protein containing a caspase recruitment domain, ASC) and effectors (caspase 1). It can detect a broad range of microbial pathogens along with foreign and host-derived danger signals, resulting in the assembly and activation of the NLRP3 inflammasome. Upon activation, NLRP3 inflammasome leads to caspase 1-dependent secretion of the pro-inflammatory cytokines IL-1β and IL-18, as well as to gasdermin D-mediated pyroptotic cell death. NLRP3 inflammasome is highly expressed in CNS-resident cell types, including microglia and astrocytes, and growing evidence suggests that NLRP3 inflammasome is a crucial player in the pathophysiology of several neuroinflammatory and psychiatric diseases, such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, stroke, traumatic brain injury, amyotrophic lateral sclerosis, and major depressive disorder. Thus, this review describes the molecular mechanisms of NLRP3 inflammasome activation and its crucial roles in the pathogenesis of neurological disorders.