• 한국독성학회:학술대회논문집
• /
• 한국독성학회 2002년도 Current Trends in Toxicological Sciences
• /
• pp.94-94
• /
• 2002

Oxidative stress induced by reactive oxygen and/or nitrogen species has been considered as a major cause of cellular injuries in a variety of neurodegenerative disorders including Alzheimer's disease (AD). Inflammatory as well as oxidative tissue damage has been implicated in pathophysiology of AD, and non-steroidal anti-inflammatory drugs have been reported to have beneficial effects in the treatment or prevention of AD.(omitted)

• 한국독성학회:학술대회논문집
• /
• 한국독성학회 2001년도 International Symposium on Dietary and Medicinal Antimutgens and Anticarcinogens
• /
• pp.115-115
• /
• 2001

Oxidative stress induced by reactive oxygen and/or nitrogen species has been considered as a major cause of cellular injuries in a variety of neurodegenerative disorders including Alzheimers disease (AD). Inflammatory as well as oxidative tissue damage has been associated with pathophysiology of AD, and non-steroidal anti-inflammatory drugs have been reported to have beneficial effects in the treatment or prevention of AD.(omitted)

• Toxicological Research
• /
• 제30권4호
• /
• pp.243-250
• /
• 2014

Mitochondrial integrity is critical for maintaining proper cellular functions. A key aspect of regulating mitochondrial homeostasis is removing damaged mitochondria through autophagy, a process called mitophagy. Autophagy dysfunction in various disease states can inactivate mitophagy and cause cell death, and defects in mitophagy are becoming increasingly recognized in a wide range of diseases from liver injuries to neurodegenerative diseases. Here we highlight our current knowledge on the mechanisms of mitophagy, and discuss how alterations in mitophagy contribute to disease pathogenesis. We also discuss mitochondrial dynamics and potential interactions between mitochondrial fusion, fission and mitophagy.

• 대한한방내과학회지
• /
• 제26권2호
• /
• pp.409-419
• /
• 2005

The water extract of Boyanghwanoh-tang has been used for treatment of ischemic vascular disease in oriental medicine. However, little is known about the mechanism by which the water extract of Boyanghwanoh-tang rescues cells from these damages. Therefore, this study was designed to evaluate the protective effects of Boyanghwanoh-tang on zinc-mediated cytotoxicity in H9c2 cardiomyoblast cells. This study demonstrates that, after treatment of H9c2 cells with zinc, there was a decrease in cell viability in a dose dependent manner, and there was a chromatin condensation. Zinc induced the change of cell morphology. In addition, zinc induced mitochondrial dysfunction. Zinc-induced H9c2 cell death was remarkably prevented by the pretreatment of Boyanghwanoh-tang consistently with increase of the peroxoredoxin 1, 2, 3, 5, and 6 expression. Taken together, the results suggest that zinc induced severe cell death in H9c2 cardiomyoblast cells, and that protective effects of Boyanghwanoh-tang against oxidative injuries are achieved through regulation of peroxiredoin expression.

• 한방안이비인후피부과학회지
• /
• 제23권1호
• /
• pp.1-7
• /
• 2010

Objective : Mercuric chloride is excreted in the urine and stool. Bangpungtongseong-san(BT) has been used commonly skin disease and has diuresis and excretion effect. This study is aimed to find out effects of Kami- bangpungtongseong-san(KBT) on the skin disease toxicated by mercury. Method : Experiment was conducted with No treated group(Normal group), Mercuric chloride subcutaneous injection group(Control group) and Kami-bangpungtongseong-san-treated group (Sample group). KBT Extracts were delivered orally in 7 days in sample group. We observed epithelial cell hyperplastic, angiogenesis, inflammatory cell infiltration of skin. For the charting the results, image analysis was taken. The result of image analysis was verified significance by Sigmaplot 2000(P<0.05). Result : This study shows an relieving epithelial cell hyperplastic, angiogenesis, inflammatory cell infiltration of exposure skin on mercuric chloride. Conclusion : According to the result of study, we can expect to the effect of KBT extracts' therapeutic action to tissue injuries of the mice' skin on acute mercurial toxication.

• Radiation Oncology Journal
• /
• 제1권1호
• /
• pp.103-109
• /
• 1983

47 out of 56 cases of intact uterine cervix cancer treated by radiation at the Hanyang University Hospital were followed 18 months or more after treatment. (7 patients died before 18 months, 2 cases lost to follow-up). Age distribution reveal 5 cases in 30's, 18 cases in 40's, 17 cases in 50's, 7 cases in 60's. Histologically, all cases were squamous cell type except one case of adenocarcinoma. 1. 45 cases were treated by combined external Co-60 irradiation and intracavitary irradiation by Cs-137 small sources. 1 case was treated by external irradiation only, and 1 case by intracavitary only. 2. Rectal injuries were observed in 13 cased (27.6%), 4 cases in Grade 1, 8 cased in Grade 2 and 1 cases in Grade 3 which needed surgical management. 3. Average intervals of rectal injury following treatment was 9.2 months varying from 5 to 15 months. 4. Relation between rectal injury and point A dose reveal 6 cases between 7000-7999 rad and 6 cases between 8000-8999 rad and 1 case above 9000 rad. Even though there is no direct relation between point A dose and rectal injury, it is expected that rectal injury increases as point A dose increase. 5. In the normal condition, rectal injury can't be attributed to one major cause. Radiation dose, small source distribution, general condition of patients, local anatomy of the individual patient, history of PID and previous surgery, all play complex roles.

• Biomolecules & Therapeutics
• /
• 제28권6호
• /
• pp.512-518
• /
• 2020

Stroke is a leading cause of long-term disability in ischemic survivors who are suffering from motor, cognitive, and memory impairment. Previously, we have reported suppressing LPA₅ activity with its specific antagonist can attenuate acute brain injuries after ischemic stroke. However, it is unclear whether suppressing LPA₅ activity can also attenuate chronic brain injuries after ischemic stroke. Here, we explored whether effects of LPA₅ antagonist, TCLPA5, could persist a longer time after brain ischemic stroke using a mouse model challenged with tMCAO. TCLPA5 was administered to mice every day for 3 days, starting from the time immediately after reperfusion. TCLPA5 administration improved neurological function up to 21 days after tMCAO challenge. It also reduced brain tissue loss and cell apoptosis in mice at 21 days after tMCAO challenge. Such long-term neuroprotection of TCLPA5 was associated with enhanced neurogenesis and angiogenesis in post-ischemic brain, along with upregulated expression levels of vascular endothelial growth factor. Collectively, results of the current study indicates that suppressing LPA₅ activity can provide long-term neuroprotection to mice with brain ischemic stroke.

• Asian Pacific Journal of Cancer Prevention
• /
• 제13권12호
• /
• pp.5965-5967
• /
• 2012

Cancer is now the main cause of increasing mortality throughout the world. Minor alterations in the cell cycle which are inherited and not removed by apoptosis are important rsik factors. Blood cancers are asmong the types which most readily cause death. Here in this study, usual but important factors such as age, gender, Rh and ABO blood typing, weight, and platelet counts are analyzed for impact on blood cancers. Frequencies and distributions, correlations and chi-square test were utilized in order to clarify the perspective of important factors. Our statistical results show males and females to have same risk in blood cancer but A blood type (40%) along with positive Rh (73%) had the highest risk. Low platelet counts are related to more than 80% of cases. Obesity has a statistically ignorable role in blood cancer prevalence. The fact that blood cancer cases increase during the second decade of life (45.7%) which might be because of involvement of maturation processes.

• Journal of Plant Biology
• /
• 제16권1_2호
• /
• pp.17-22
• /
• 1973

The experiments were conducted to examine the injuries of $SO_2$, $NH_3$, and $SO_2$ and NH3 mixed gas to the germination and the growth of plants. Six kinds of plants were used as the material. These plants seeds were treated with the gases for five days. Rate of the germination and the growth in height of varying plants were different according to the components of the gases. The critical concentration of the gases for both the germination and the growth were in 5ppm of $SO_2$, 50ppm of $NH_3$, and 50ppm $SO_2$ and 50ppm $NH_3$ mixed gases. When a low concentration of $SO_2$ was treated together with NH3, especially it was reduced to 60 percent of the damage in the germination and the growth. In the treatemnt with $SO_2$, the germination of the seeds which soaked in water for 24 hours reduced the injuries more 40 percent than those which for one hour. It was observed that the seeds with thick coasts or with originally intact coats were suffered but little damaged by the gases, and the external symptoms of an injury were shown, at first, in water pore, and then, in guard cell on the leaves.

• The Korean Journal of Physiology and Pharmacology
• /
• 제25권5호
• /
• pp.425-437
• /
• 2021

Although the contributions of sitagliptin to endothelial dysfunction in diabetes mellitus were previously reported, the mechanisms still undefined. Autophagy plays an important role in the development of diabetes mellitus, but its role in diabetic macrovascular complications is unclear. This study aims to observe the effect of sitagliptin on macrovascular endothelium in diabetes and explore the role of autophagy in this process. Diabetic rats were induced through administration of high-fat diet and intraperitoneal injection of streptozotocin. Then diabetic rats were treated with or without sitagliptin for 12 weeks. Endothelial damage and autophagy were measured. Human umbilical vein endothelial cells were cultured either in normal glucose or in high glucose medium and intervened with different concentrations of sitagliptin. Rapamycin was used to induce autophagy. Cell viability, apoptosis and autophagy were detected. The expressions of proteins in c-Jun N-terminal kinase (JNK)-Bcl-2-Beclin-1 pathway were measured. Sitagliptin attenuated injuries of endothelium in vivo and in vitro. The expression of microtubuleassociated protein 1 light chain 3 II (LC3II) and beclin-1 were increased in aortas of diabetic rats and cells cultured with high-glucose, while sitagliptin inhibited the over-expression of LC3II and beclin-1. In vitro pre-treatment with sitagliptin decreased rapamycin-induced autophagy. However, after pretreatment with rapamycin, the protective effect of sitagliptin on endothelial cells was abolished. Further studies revealed sitagliptin increased the expression of Bcl-2, while inhibited the expression of JNK in vivo. Sitagliptin attenuates injuries of vascular endothelial cells caused by high glucose through inhibiting over-activated autophagy. JNK-Bcl-2-Beclin-1 pathway may be involved in this process.