• Title/Summary/Keyword: Ischemic Damage

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A study of the Mori Radicis Cortex pre-treatment on transient ischemic brain injury in mice (상백피(桑白皮) 메탄올 추출물 전처치가 일과성 허혈에 의한 생쥐의 뇌 손상에 미치는 영향)

  • Chung, Byung-Woo;Lim, Jae-Yu;Lee, Se-Eun;Lee, Byoungho;Lim, Sehyun;Lim, Chiyeon;Cho, Suin
    • The Korea Journal of Herbology
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    • v.32 no.1
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    • pp.25-31
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    • 2017
  • Objectives : Mori Radicis Cortex (MRC), the root epidermis of Morus alba L., has been traditionally used to treat lung-related diseases in Korean Medicine. The common of MRC is Mulberry bark Morus bark, and it's pharmaceutical properties and taste are known as sweet and cold, and it promotes urination and reduce edema by reducing heat from the lungs and soothe asthma. In the present study, anti-apoptotic mechanism of MRC in middle cerebral artery occlusion (MCAO) model in mice. Methods : Two-hundred grams of MRC was extracted with methanol at room temperature for 5 days, and this was repeated one time. After filtration, the methanol was removed using vacuum evaporator, then stored at $-20^{\circ}C$ until use. C57BL/6 male mice were housed in an environment with controlled humidity, temperature, and light cycle. In order to determine beneficial effects of MRC on ischemia induced brain damage, infarct volume, neurological deficit scores, activities of several apoptosis-related proteins such as caspase-8, -9, Bcl-xL in MCAO-induced brains of mice were analyzed. Mice in MRC-treated groups were orally administered 30, 100, or 300 mg/kg of body weight for three consecutive days before commencing the MCAO procedure. Results : Pre-treatment of MRC significantly reduced infarct volume in MCAO subjected mice applied with 300 mg/kg of MRC methanol extract, and MRC effectively inhibited Bcl-xL reduction and caspase-9 activation caused by MCAO-induced brain damage. Conclusions : MRC showed neuro-protective effects by regulating apoptosis-related protein signals, and it can be a potential candidate for the therapy of ischemia-induced brain damage.

Cardioprotection via mitochondrial transplantation supports fatty acid metabolism in ischemia-reperfusion injured rat heart

  • Jehee Jang;Ki-Woon Kang;Young-Won Kim;Seohyun Jeong;Jaeyoon Park;Jihoon Park;Jisung Moon;Junghyun Jang;Seohyeon Kim;Sunghun Kim;Sungjoo Cho;Yurim Lee;Hyoung Kyu Kim;Jin Han;Eun-A Ko;Sung-Cherl Jung;Jung-Ha Kim;Jae-Hong Ko
    • The Korean Journal of Physiology and Pharmacology
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    • v.28 no.3
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    • pp.209-217
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    • 2024
  • In addition to cellular damage, ischemia-reperfusion (IR) injury induces substantial damage to the mitochondria and endoplasmic reticulum. In this study, we sought to determine whether impaired mitochondrial function owing to IR could be restored by transplanting mitochondria into the heart under ex vivo IR states. Additionally, we aimed to provide preliminary results to inform therapeutic options for ischemic heart disease (IHD). Healthy mitochondria isolated from autologous gluteus maximus muscle were transplanted into the hearts of Sprague-Dawley rats damaged by IR using the Langendorff system, and the heart rate and oxygen consumption capacity of the mitochondria were measured to confirm whether heart function was restored. In addition, relative expression levels were measured to identify the genes related to IR injury. Mitochondrial oxygen consumption capacity was found to be lower in the IR group than in the group that underwent mitochondrial transplantation after IR injury (p < 0.05), and the control group showed a tendency toward increased oxygen consumption capacity compared with the IR group. Among the genes related to fatty acid metabolism, Cpt1b (p < 0.05) and Fads1 (p < 0.01) showed significant expression in the following order: IR group, IR + transplantation group, and control group. These results suggest that mitochondrial transplantation protects the heart from IR damage and may be feasible as a therapeutic option for IHD.

Ischemic Time Associated with Activation of Rejection-Related Immune Responses (허혈 시간과 거부반응 관련 면역반응)

  • Nam, Hyun-Suk;Choi, Jin-Yeung;Kim, Yoon-Tai;Kang, Kyung-Sun;Kwon, Hyuk-Moo;Hong, Chong-Hae;Kim, Doo;Han, Tae-Wook;Moon, Tae-Young;Kim, Jee-Hee;Cho, Byung-Ryul;Woo, Heung-Myong
    • Journal of Veterinary Clinics
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    • v.26 no.2
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    • pp.138-143
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    • 2009
  • Ischemia/reperfusion injury(I/RI) is the major cause of acute renal failure and delayed graft function(DGF) unavoidable in renal transplantation. Enormous studies on ischemia damage playing a role in activating graft rejection factors, such as T cells or macrophages, are being reported. Present study was performed to determine whether ischemia time would play an important role in activating rejection-related factors or not in rat models of I/RI. Male Sprague-Dawley rats were submitted to 30, 45, and 60 minutes of warm renal ischemia with nephrectomy or control animals underwent sham operation(unilateral nephrectomy). Renal function and survival rates were evaluated on day 0, 1, 2, 3, 5 and 7. Immunofluorescence staining of dendritic cells(DCs), natural killer(NK) cells, macrophages, B cells, CD4+ and CD8+ T cells were measured on day 1 and 7 after renal I/RI. Survival rates dropped below 50% after day 3 in 45 minutes ischemia. Histologic analysis of ischemic kidneys revealed a significant loss of tubular architecture and infiltration of inflammatory cells. DCs, NK cells, macrophages, CD4+ and CD8+ T cells were infiltrated from a day after I/RI depending on ischemia time. Antigen presenting cells(DCs, NK cells or macrophages) and even T cells were infiltrated 24 hours post-I/RI, which is at the time of acute tubular necrosis. During the regeneration phase, not only these cells increased but B cells also appeared in more than 45 minutes ischemia. The numbers of the innate and the adaptive immune cells increased depending on ischemia as well as reperfusion time. These changes of infiltrating cells resulting from each I/RI model show that ischemic time plays a role in activating rejection related immune factors and have consequences on progression of renal disease in transplanted and native kidneys.

Pneumatosis Cystoides Intestinales and Portomesenteric Venous Gas following Anticholinesterase Pesticide Poisoning (항콜린에스테라아제 살충제 음독 후 발생한 창자벽공기낭증과 문맥장간막정맥가스 1례)

  • Lee, Suk Hee;Lee, Kyung-Woo;Jung, Jin Hee
    • Journal of The Korean Society of Clinical Toxicology
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    • v.15 no.1
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    • pp.56-59
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    • 2017
  • Pneumatosis cystoides intestinalis and portomesenteric venous gas are uncommon radiological findings, but are found commonly in cases of bowel ischemia, or as a result of various non-ischemic conditions. A 72-year-old man visited an emergency center with altered mental status 2 hours after ingestion of an unknown pesticide. On physical examination, he showed the characteristic hydrocarbon or garlic-like odor, miotic pupils with no response to light, rhinorrhea, shallow respiration, bronchorrhea, and sweating over his face, chest and abdomen. Laboratory results revealed decreased serum cholinesterase, as well as elevated amylase and lipase level. We made the clinical diagnosis of organophosphate poisoning in this patient based on the clinical features, duration of symptoms and signs, and level of serum cholinesterase. Activated charcoal, fluid, and antidotes were administered after gastric lavage. A computerized tomography scan of the abdomen with intravenous contrast showed acute pancreatitis, poor enhancement of the small bowel, pneumatosis cystoides intestinalis, portomesenteric venous gas and ascites. Emergent laparotomy could not be performed because of his poor physical condition and refusal of treatment by his family. The possible mechanisms were believed to be direct intestinal mucosal damage by pancreatic enzymes and secondary mucosal disruption due to bowel ischemia caused by shock and the use of inotropics. Physicians should be warned about the possibility of pneumatosis cystoides intestinalis and portomesenteric venous gas as a complication of pancreatitis following anticholinesterase poisoning.

Development of Healthcare Data Quality Control Algorithm Using Interactive Decision Tree: Focusing on Hypertension in Diabetes Mellitus Patients (대화식 의사결정나무를 이용한 보건의료 데이터 질 관리 알고리즘 개발: 당뇨환자의 고혈압 동반을 중심으로)

  • Hwang, Kyu-Yeon;Lee, Eun-Sook;Kim, Go-Won;Hong, Seong-Ok;Park, Jung-Sun;Kwak, Mi-Sook;Lee, Ye-Jin;Lim, Chae-Hyeok;Park, Tae-Hyun;Park, Jong-Ho;Kang, Sung-Hong
    • The Korean Journal of Health Service Management
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    • v.10 no.3
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    • pp.63-74
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    • 2016
  • Objectives : There is a need to develop a data quality management algorithm to improve the quality of healthcare data using a data quality management system. In this study, we developed a data quality control algorithms associated with diseases related to hypertension in patients with diabetes mellitus. Methods : To make a data quality algorithm, we extracted the 2011 and 2012 discharge damage survey data from diabetes mellitus patients. Derived variables were created using the primary diagnosis, diagnostic unit, primary surgery and treatment, minor surgery and treatment items. Results : Significant factors in diabetes mellitus patients with hypertension were sex, age, ischemic heart disease, and diagnostic ultrasound of the heart. Depending on the decision tree results, we found four groups with extreme values for diabetes accompanying hypertension patients. Conclusions : There is a need to check the actual data contained in the Outlier (extreme value) groups to improve the quality of the data.

Neuroprotective Effects of Some Plant Extracts against Oxygen-Glucose Deprivation (OGD)-Induced Oxidative Cell Death on Neuronal Cell (산소-포도당 결핍(OGD) 유도성 신경세포 사멸에 대한 뇌 보호 효과를 가지는 수종 생약추출물의 검색)

  • Lee, Hak-Ju;Koo, Uk;Lee, Hyun-Jung;Lee, Dong-Ho;Mar, Woong-Chon
    • Korean Journal of Medicinal Crop Science
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    • v.17 no.5
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    • pp.341-345
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    • 2009
  • Cerebral ischemia results from a transient or permanent reduction in cerebral blood flow that decreases oxygen and glucose supply. When the cellular oxygen supply is reduced to critical level, damage to cells and induction of cell death are occurred by excitotoxicity, oxidative stress and inflammation. Ischemia remains one of the leading causes of death, but there is no effective treatment that might protect neurons gainst ischemia by interrupting the cascade of cell death. In this study, human neuroblastoma SH-SY5Y cells are exposed to oxygen and glucose deprivation (OGD) followed by reoxgenation. OGD can mimic the acute restriction of metabolite and oxygen supply caused by ischemia and is widely used as a model of ischemic conditions. SH-SY5Y cells are treated samples at the commencement of OGD to achieve different final concentrations, and cell viabilities were quantified using the measurement of flow cytometry analysis. Of those tested, the extracts of Polygala tenuifolia (roots), Dictamnus dasycarpus (barks), Polygala tenuifolia (roots), Eucommia ulmoides (branches), Eucommia ulmoides (barks), Poria cocos (whole), Sophora flavescens (roots) showed neuroprotective effects, with $EC_{50}$ values of $4.5{\pm}0.6$, $7.9{\pm}1.5$, $10.5{\pm}0.7$, $18.4{\pm}1.9$, $19.6{\pm}0.3$, $21.6{\pm}1.9$, and $30.7{\pm}3.9{\mu}g/m{\ell}$, respectively.

Increase of Synapsin I, Phosphosynapsin (ser-9), and GAP-43 in the Rat Hippocampus after Middle Cerebral Artery Occlusion

  • Jung, Yeon-Joo;Huh, Pil-Woo;Park, Su-Jin;Park, Jung-Sun;Lee, Kyung-Eun
    • The Korean Journal of Physiology and Pharmacology
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    • v.8 no.2
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    • pp.77-81
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    • 2004
  • The loss of neurons and synaptic contacts following cerebral ischemia may lead to a synaptic plastic modification, which may contribute to the functional recovery after a brain lesion. Using synapsin I and GAP-43 as markers, we investigated the neuronal cell death and the synaptic plastic modification in the rat hippocampus of a middle cerebral artery occlusion (MCAO) model. Cresyl violet staining revealed that neuronal cell damage occurred after 2 h of MCAO, which progressed during reperfusion for 2 weeks. The immunoreactivity of synapsin I and GAP-43 was increased in the stratum lucidum in the CA3 subfield as well as in the inner and outer molecular layers of dentate gyrus in the hippocampus at reperfusion for 2 weeks. The immunoreactivity of phosphosynapsin was increased in the stratum lucidum in the CA3 subfield during reperfusion for 1 week. Our data suggest that the increase in the synapsin I and GAP-43 immunoreactivity probably mediates either the functional adaptation of the neurons through reactive synaptogenesis from the pre-existing presynaptic nerve terminals or the structural remodeling of their axonal connections in the areas with ischemic loss of target cells. Furthermore, phosphosynapsin may play some role in the synaptic plastic adaptations before or during reactive synaptogenesis after the MCAO.

Experimental Study on the Effect of Temporary Clipping on the Histological Changes of the Arterial Walls of Rats

  • Koh, Hyeon-Song;Kwon, O-Yu
    • Biomedical Science Letters
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    • v.13 no.2
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    • pp.111-117
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    • 2007
  • Temporary occlusion of the parent artery or feeding artery is an useful method in microsurgery for cerebrovascular diseases. The advantages of the temporary clipping for intracranial aneurysm surgery have already been proven by many experimental and clinical reports. Currently, there are two methods of temporary clipping: 1) intermittent clipping, 2) continuous clipping. In many previous studies, the intermittent, repeated clipping technique was reported to reduce ischemic damage to the brain, but it is still debated. On the other hand, a comparison of the histological changes on the arterial wall between each clipping method has not been sufficiently reported yet. So the authors performed experimental temporary clipping on the common carotid and femoral arteries of about 25 rats using the Sugita temporary mini-clip. The specimens were divided into two major groups and seven subgroups: Group I (I-1, I-2, I-3, I-4, intermittent clippings for 5 minutes were done once, twice, three times, and few times), and Group C (C-10, C-15, C-20, continuous clippings for 10, 15, 20 minutes, respectively). The reperfusion time after the temporary clipping was the same as the clipping duration. Under light microscope, the histological findings by Hematoxylin-Eosin staining were examined in all specimens, which were obtained at each time interval after temporary clipping. Then the histological changes of the arterial walls by two different methods were compared with the normal specimen. The results suggest that intermittent temporary clipping is less damaging on the arterial wall than single continuous clipping.

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Protective Effects of Hwangryunhaedog-tang on Hypoxia-induced Apoptosis in H9c2 Cardiomyoblast Cells (황연해독탕이 저산소증에 의한 배양심근세포고사에 미치는 영향)

  • Jeong Jae Eun;Yu Bong Seon;Park Jin Yeong;Jeon In Cheol;Park Sang Beom;Lee Dae Yong;Lee Min Goo;Lee In;Moon Byun Soon
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.18 no.6
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    • pp.1733-1739
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    • 2004
  • The water extract of Hwangryunhaedog-tang(HRHDT} has been traditionally 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 HRHDT rescues cells from these damages. This study was designed to investigate the protective mechanisms of HRHDT on hypoxia-induced cytotoxicity in H9c2 cardiomyoblast cells. Hypoxia, markedly decreased the viability of H9c2 cells, which was characterized with apparent apoptptic features such as chromatin condensation as well as fragmentation of genomic DNA and nuclei. However, HRHDT significantly reduced hypoxia-induced cell death and apoptotic characteristics. Also, HRHDT prevented the mitochondrial dysfunction including the disruption of mitochondria membrane permeability transition (MPT) and an increase in expression of anti-apoptotic Bcl-2 proteins in hypoxia-H9c2 cells. Taken together, this study suggests that the protective effects of the water extract of HRHDT against hypoxic damages may be mediated by the modulation of Bcl-2 and Bak expression.

Experimental Study on Cavo-Pulmonary Anastomosis (상공정맥-우폐동맥 문합에 관한 실험적 연구)

  • 양기민
    • Journal of Chest Surgery
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    • v.10 no.2
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    • pp.281-294
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    • 1977
  • Superior vena cava to pulmonary arterial shunting operation was made between the superior vena cava and the right pulmonary artery in the fashion of end-to-end anastomosis in 20 mongrel dogs. The experimental animals were divided into three group and blood flow in the superior vena cava was occluded for 20, 30 and 60 minutes respectively, and observations were made for the changes in caval pressure and cerebrospinal fluid pressure. And pathologic examinations were also performed. On occluding the caval blood flow, the superior vena caval pressure was sharply and immediately elevated from $103.5{\pm}19.8mmH_2O$ at thoracotomy to $556.4{\pm}86.lmmH_2O$ within 2 minutes to make its plateau thereafter, and the cerebrospinal fluid pressure followed closely the changes of the superior vena caval pressure in its level and pattern being elevated from $102.0{\pm}19.9mmH_2O$ to $490.5{\pm}79.9mmH_2O$. The drops of both the caval and cerebrospinal fluid pressures were definite and marked on opening the shunt flow through the anastomosis, but these postoperative pressures retained still higher ones above their levels measured at thoracotomy. The pathological examinations of the brain and the spinal cord were also performed in six animals. Characteristic changes uniformly seen in all area and in all animals were the findings of capillary congestion and perivascular edema. On the other hand, ischemic nerve cell changes were rather evident, revealing their degrees and extents being related to the prolongation of the time of caval occlusion which has followed by the sustained high pressures in both the superior vena and the cerebrospinal fluid. The experiment suggests the safety of this surgical procedure with minimal, if any, permanent damage as long as the occlusion of the caval blood flow is not prolonged beyond the expected.

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