• Journal of the Korea Academia-Industrial cooperation Society
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• v.19 no.2
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• pp.456-461
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• 2018

Carotid artery stenting (CAS) has emerged as an alternative treatment for carotid stenosis in patients poorly suited for endarterectomy. Intracerebral hemorrhage following carotid revascularization (endarterectomy, angioplasty, artery stenting) is rare and thought to be related to reperfusion injury in most cases. Early experience suggests an increased incidence of hemorrhage following CAS as compared to endarterectomy. In this study, data were obtained through a case report on an 80-year-old male patient with cerebral infarction. The 80-year-old hypertensive man developed sudden monoparesis in the left arm. He underwent CAS for 90% stenosis of the left proximal internal carotid artery. Brain CT after procedure showed acute hematoma with left posterior cerebral artery territorial hemorrhage, including the upper thalamus with extended intraventricular hemorrhage (IVH). Since this hemorrhage occurred in vascular territory unlikely to have been supplied by the treated artery, this case suggests that the mechanism of intracerebral hemorrhage following CAS may in some cases be different from hyperperfusion hemorrhage classically described following endarterectomy.

• Journal of Korean Physical Therapy Science
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• v.8 no.1
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• pp.745-758
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• 2001

The purpose of study to phenomenological examine and the mechanism regarding the gene(DNA, RNA, Protein) and sports to studied, analyzed. and evaluated. This review considers the evidence for genetic effects in several determinants of endurance performance and resistance performance, namely: body measurements and physique, body fat pulmonary functions, cardiac and circulatory functions, muscle characteristics. substrate utilization, maximal aerobic power and other. Moreover, the response to aerobic training of indicators aerobic work metabolism and endurance performance is reviewed, with emphasis on the specificity of the response and the individual differences observed in training ability. This study indicate that improvement of 'Enhancer Action' in RNA genes changed by exercise or sports. Moreover exercise was effect on Central Dogma with DNA makes RNA makes Protein. and think that occurred with exercise influence on skeletal muscle into cell have to Myosin Heavy Chain (MHC) changed was after exercise performance, which accompanied into skeletal muscle that were exercise-induces gene-modulation that is, take gene mutations. This study known that existed hormone(epinephrine)-immune system with interaction. Exercise were altered insulin binding and MAP Kinase signaling increased into immune cells. This review suggested that the high rate of glutamine utilization by cells of the immune system serves to maintain a high intra cellular concentration of the intermediates of biosynthetic pathways such that optimal rates of DNA, RNA and protein synthesis can be maintained. In the absence of glutamine, lymphocytes do not proliferate in vitro: proliferation increase greatly as the glutamine concentration increase. Glutamine is synthesized in skeletal muscle. Skeletal muscle and plasma glutamine levels are lowered by sepsis, injury, bums, surgery and endurance exercise and in the overtrained athlete. The study of result show that production of ET-1 is markedly increased tissue specifically in the heart by exercise without appreciable changes in endothelin-converting enzyme and endothelial receptor expressions, suggest that myocardial ET-1 may participate in modulation of cardiac function during exercise. Conclusionally, this study indicate that improvement of 'Enhancer Action' in RNA genes changed by exercise or sports. Moreover exercise was effect on Central Dogma with DNA makes RNA makes Protein. This study is expected to contribute the area of sports science, medicine, hereafter more effort is required to establish the relation between gene alters and exercise amount.

• Applied Biological Chemistry
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• v.51 no.2
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• pp.129-135
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• 2008

Berberine is an isoquinoline alkaloid used in traditional Chinese medicine and has been isolated from a variety of plants, such as Coptis chinensis and Phellodendron amurense. It has a wide spectrum of clinical applications such as in anti-tumor, anti-microbial, and anti-inflammatory activities. However, it is still unknown that berberine related with reactive oxygen species (ROS)-mediated apoptosis pathway in human hepatoma HepG2 cells. In the present study, we are examined the molecular mechanism of ROS- and p38 MAP kinase-mediated apoptosis by berberine in HepG2 cells. Berberine increased cytotoxicity effects by time- and does-dependent manner. $LD_{50}$ was detected 50 ${\mu}M$ at 48h of exposure to berberine. Nuclei cleavage and apoptotic DNA fragmentation were observed in cells treated with 50 ${\mu}M$ of berberine for 48h. Moreover, berberine induced the activating of caspase-3, p53, p38 and Bax expression, whereas the expression of anti-apoptotic signaling pathways, Bcl-2, was decreased. Additionally, berberine-treated cells had an increased level of generation of ROS and nitric oxide (NO). These results indicated that berberine induces apoptosis of HepG2 cells may be mediated oxidative injury acts as an early and upstream change, triggers mitochondrial dysfunction, Bcl-2 and Bax modulation, p38 and p53 activation, caspase-3 activation, and consequent leading to apoptosis.

• The Korean Journal of Physiology and Pharmacology
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• v.11 no.2
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• pp.65-70
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• 2007

Chinese herb medicines have traditionally been used to treat or alleviate the symptom of various diseases. The rationale for use of certain herbs to certain disorder is now getting unveiled by modern technology. In the present study, we investigated whether herb mix extract(HMX), which is alleged to be useful for gastric ulcer, protects stomach from oxidative stress. Rats were allowed to normal diet with and without HMX (1, 5, 10 mg/kg) for 30 days. To induce gastric ulcer, ethanol (75%, 1.5 ml) or acidified aspirin (100 mg/kg in 0.2 N HCl) was administered by oral route in 24 h-fasted rats and examined the gastric ulceration(bleeding) by measuring the size 1 h after the treatment. Results indicated the area of gastric bleeding was significantly less in HMX fed rats than in normal diet fed ones, and it was dependent on the duration and amount of HMX. To investigate the underlying mechanism by which HMX protects stomach from oxidative stress, expression of enzymes like heme oxygenase (HO), cyclooxygenase (COX), and inducible nitric oxide (iNOS) were investigated in MKN-74 cells, where aspirin or H. pylori was introduced. The results were compared with RAW 264.7 cells to check if there's cell specificities exist. The expression of HO-1 but not COX-2, iNOS was significantly increased by HMX. Furthermore, HO-1 inhibitor, SnPP IX reduced the HO-1 activity and reversed the survival rate in HMX-treated MKN-74 cells. There's no difference between RAW 264.7 cells and MKN-74 cells. We, thus, concluded that HMX is beneficial for protection from oxidative injury, and induction of HO-1 by HMX in gastric cells is, at least, responsible for protection from oxidative stress such as ethanol, aspirin and possibly H. pylori infection.

• The Korean Journal of Physiology and Pharmacology
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• v.11 no.2
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• pp.57-64
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• 2007

Ischemic preconditioning (IPC) is known to protect the heart against ischemia/reperfusion (IR)-induced injuries, and regional differences in the mitochondrial antioxidant state during IR or IPC may promote the death or survival of viable and infarcted cardiac tissues under oxidative stress. To date, however, the interplay between the mitochondrial antioxidant enzyme system and the level of reactive oxygen species (ROS) in the body has not yet been resolved. In the present study, we examined the effects of IR- and IPC-induced oxidative stresses on mitochondrial function in viable and infarcted cardiac tissues. Our results showed that the mitochondria from viable areas in the IR-induced group were swollen and fused, whereas those in the infarcted area were heavily damaged. IPC protected the mitochondria, thus reducing cardiac injury. We also found that the activity of the mitochondrial antioxidant enzyme system, which includes manganese superoxide dismutase (Mn-SOD), was enhanced in the viable areas compared to the infarcted areas in proportion with decreasing levels of ROS and mitochondrial DNA (mtDNA) damage. These changes were also present between the IPC and IR groups. Regional differences in Mn-SOD expression were shown to be related to a reduction in mtDNA damage as well as to the release of mitochondrial cytochrome c (Cyt c). To the best of our knowledge, this might be the first study to explore the regional mitochondrial changes during IPC. The present findings are expected to help elucidate the molecular mechanism involved in IPC and helpful in the development of new clinical strategies against ischemic heart disease.

• Tuberculosis and Respiratory Diseases
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• v.80 no.3
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• pp.247-254
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• 2017

Background: Airway epithelial cells are the first line of defense, against pathogens and environmental pollutants, in the lungs. Cellular stress by cadmium (Cd), resulting in airway inflammation, is assumed to be directly involved in tissue injury, linked to the development of lung cancer, and chronic obstructive pulmonary disease (COPD). We had earlier shown that ACN9 (chromosome 7q21), is a potential candidate gene for COPD, and identified significant interaction with smoking, based on genetic studies. However, the role of ACN9 in the inflammatory response, in the airway cells, has not yet been reported. Methods: We first checked the anatomical distribution of ACN9 in lung tissues, using mRNA in situ hybridization, and immunohistochemistry. Gene expression profiling in bronchial epithelial cells (BEAS-2B), was performed, after silencing ACN9. We further tested the roles of ACN9, in the intracellular mechanism, leading to Cd-induced production, of proinflammatory cytokines in BEAS-2B. Results: ACN9 was localized in lymphoid, and epithelial cells, of human lung tissues. ACN9 silencing, led to differential expression of 216 genes. Pathways of sensory perception to chemical stimuli, and cell surface receptor-linked signal transduction, were significantly enriched. ACN9 silencing, further increased the expression of proinflammatory cytokines, in BEAS-2B after Cd exposure. Conclusion: Our findings suggest, that ACN9 may have a role, in the inflammatory response in the airway.

• Journal of Dental Anesthesia and Pain Medicine
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• v.17 no.1
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• pp.37-46
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• 2017

Background: In oxidative stress, reactive oxygen species (ROS) production contributes to cellular dysfunction and initiates the apoptotic cascade. Autophagy is considered the mechanism that decreases ROS concentration and oxidative damage. Propofol shows antioxidant properties, but the mechanisms underlying the effect of propofol preconditioning (PPC) on oxidative injury remain unclear. Therefore, we investigated whether PPC protects against cell damage from hydrogen peroxide ($H_2O_2$)-induced oxidative stress and influences cellular autophagy. Method: COS-7 cells were randomly divided into the following groups: control, cells were incubated in normoxia (5% $CO_2$, 21% $O_2$, and 74% $N_2$) for 24 h without propofol; $H_2O_2$, cells were exposed to $H_2O_2$ ($400{\mu}M$) for 2 h; $PPC+H_2O_2$, cells pretreated with propofol were exposed to $H_2O_2$; and 3-methyladenine $(3-MA)+PPC+H_2O_2$, cells pretreated with 3-MA (1 mM) for 1 h and propofol were exposed to $H_2O_2$. Cell viability was determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide thiazolyl blue (MTT) reduction. Apoptosis was determined using Hoechst 33342 staining and fluorescence microscopy. The relationship between PPC and autophagy was detected using western blot analysis. Results: Cell viability decreased more significantly in the $H_2O_2$ group than in the control group, but it was improved by PPC ($100{\mu}M$). Pretreatment with propofol effectively decreased $H_2O_2$-induced COS-7 cell apoptosis. However, pretreatment with 3-MA inhibited the protective effect of propofol during apoptosis. Western blot analysis showed that the level of autophagy-related proteins was higher in the $PPC+H_2O_2$ group than that in the $H_2O_2$ group. Conclusion: PPC has a protective effect on $H_2O_2$-induced COS-7 cell apoptosis, which is mediated by autophagy activation.

• The Journal of Internal Korean Medicine
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• v.19 no.1
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• pp.144-156
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• 1998

This study has been carried out to investigate the cause, pathological mechanism and treatment of symptoms regarded as the ischemic heart disease in Nei-jing(內經). I've got the following conclusions. 1. From the side of xing-bi(胸痺), the ischemic heart disease(IHD) was caused by that the energy in one's heart wasn't extended in the way of Yin-xie(飮邪), namely waste matter of human body and symptoms and treatment wern't written. 2. From the side of xin-bi (心痺), HID was catched by the mechanisms that the blood vessel is blocked. or the heart's blood was deficient owing to the mutation of mo-bi(脈痺), the lack of yang-ming(陽明) and excessive thoughts and worry and others. The symptoms were feeling oppressed in one's brest, palpitating, sudden dyspnea, the dryness of thorat, frequent belching and the fear by the inverse flow of the energy(氣). The treatment was that the yin(陰) was cured immediately, but the yang(陽) mustn't be attacked. 3. From the side of xing-tong(心痛), IHD was suffered from by mechanisms that following the han-sa(寒邪), namely the cold makes a invasion on humanbody, the vessel was blocked, spasm, filled and the amount of blood flow was poor, or caused by injury of vessel, the inverse flow and the disease of shi-dong(是動病) of shou-shao-xin-jing(手少陰心經) and so on. The pain was cramped into the upper and lower back or lower abdomen or throat and accompanied with nausea, abdominal dropsy, constipation, the impending of breathing and so on. The cure was mainly that acupuncture was applied at the jin-su(筋縮) region or meridian in relation to symptoms, but if the pain were severe, acupuncture mustn't be applied. The prog nosis was worse. 4. From the side of xing-tonge(心痛), IHD was divided into zhen-xing-tong(眞心痛) and jue-xing-tong(厥心痛), but pi-xiog-tong(脾心痛) and wei-xing-tong(胃心痛) out of jue-xing-tong(厥心痛) also included the symptoms of the digestive disease.

• Korean Journal of Veterinary Research
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• v.46 no.4
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• pp.327-335
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• 2006

A stable and reliable Helicobacter pylori (H. pylori) infection animal model would be necessary for evaluating vaccine efficacy and helpful for understanding the pathological mechanism of the organism. The aim of the present study is to investigate the effect of ethanol treatment prior to H. pylori inoculation on associated gastric mucosal injury and to establish ethanol-pretreating animal model to study H. pylori infection. Male Mongolian gerbils were used for the study. H. pylori was orally inoculated after 12 h fasting. 3 h prior to H. pylori inoculation, a group of gerbils was orally treated with absolute ethanol, 60% and 40% ethanol respectively. Another group of animals was treated either with H. pylori culture media alone or with different concentrations of ethanol plus culture media. Gerbils were killed 4 or 8 weeks after H. pylori inoculation. The colonization of H. pylori was confirmed by both histological examination and rapid urease test. Mucosal damage was evaluated grossly and histologically according to the criteria. The colonization of H. pylori and pathological changes in gastric mucosa of the animals were also observed. Although no significant change to the gastric mucose was observed in the animals treated either with H. pylori culture media alone or with different concentrations of ethanol plus culture media, persistent H. pylori infection was seen in the mucosa and mucosal leucocyte infiltration and severe epithelial damage was observed in the Helicobacter and ethanol + Helicobacter groups after 4 weeks. The gross and histological scores were higher in the ethanol + Helicobacter than in the Helicobacter alone group. As the results, ethanol-pretreatment with 60% concentration induced severe pathogenic changes by H. pylori infection in 5 weeks-old Mongolian gerbils. These results suggested that ethanol-pretreatment before H. pylori inoculation could increase the severity of gastric mucosal inflammation and enhance the colonization of H. pylori. The established ethanol-pretreating animal model would contribute to screen new drugs against H. pylori and be used as an useful tool for various animal experiments with H. pylori strains.

• Applied Biological Chemistry
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• v.32 no.1
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• pp.23-29
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• 1989

Biochemical consequence of the accumulation in cells of superoxide $(O^{-}_{2})$ which was proposed to be probably a common chemical factor in the secondary process of the mechanism of chilling injury as well as in the visible light photodamage in cells of higher plants, has been investigated in the present work. Especially focused was the destructive effect of $O^{-}_{2}$ on the biochemical activity of mitochondria, as informations which support the suggestion that mitochondrial inner membrane is the major site of $O^{-}_{2}$ production have been collected. Mitochondria and submitochondrial particles (SMP) were prepared from soybean hypocotyls for this case study. When SMP were treated with the electrolytically produced $O^{-}_{2}$ they suffered not only inhibition of the membrane-bound enzymes as demonstrated by cytochrome c oxidase, but also lipid peroxidation of membrane as proved by malondialdehyde production. Malate dehydrogenase present in the protein extract from mitochondrial matrix was also inhibited by the $O^{-}_{2}$ treatment. These results exhibited the chaotic effect of the overproduction and accumulation of $O^{-}_{2}$ in cells under a certain abnormal circumstance such as environmental stress on the physiological function of mitochondrial; disruption of the cellular metabolic pathways and the structural integrity of membrane.