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Phenobarbital 및 인진호투여가 四鹽化炭素에 依한 急性 中毒性 肝病變에 미치는 影響에 關한 病理組織學的 硏究
鄭昊錫,姜大榮 충남대학교 의과대학 지역사회의학연구소 1985 충남의대잡지 Vol.12 No.1
Carbon tetrachloride, a potent hepatotoxic agent, is mainly metabolized in the liver, and its hepatotoxic action is influenced by the administration of phenobarbital or artemisia messerschimidtiana besser var. viridis(artemisia). Artemisia was used as folk medicine for the treatment of hyperbilirubinemia or patient with acute hepatitis. Sprague-Dawley rats(male and female) were administrated with 2 ml of carbon tetrachloride (CCI_4-olive oil 1 : 4 solution) intraperitoneally, after being anesthetized by ether. After 24 hours, phenobarbital(50 mg/kg/day) and artemisia (0.6 ml/kg/day) were admin istrated intraperitoneally for 3 days. Food was withheld 12 hours before CCI_4, administration. 7 animals of each group were sacrificed at 4th, 5th, 6th and 7 th day after CCI_4 injection. The histopathological changes in the liver cells of the control and experimental groups were noted as follows; 1. Vacuolar degeneration of the hepatic cells of CCl_4-phenobarbital administrated rats showed more marked in degree than the control, and that of CCl_4-artemisia administrated rats is milder than the control. 2. Fatty change of the hepatic cells of CCl_4,-phenobarbital administrated rats showed more marked in degree than the control, and that of CCl_4-artemisia administrated rats is milder than the control. 3. The necrotic changes of the hepatic cells of CCl_4,-phenobarbital administrated rats showed more marked in degree and remained longer than the control. Temporarily, that of CCl_4-artemisia administrated rats showed more marked in degree than control, but early recovered.
Chloroform 만성 중독으로 인한 간병변에 대한 병리학적 연구
정호석,강대영 忠南大學校 癌共同硏究所 1991 癌共同硏究所 硏究誌 Vol.1 No.1
In an attempt to elucidate the pathological effects of chloroform(CHCl_(3)) administration, the present study was undertaken in male Sprague-Dawley rats. Evidence for the existence of hyperplastic nodules, oval cells, bile duct or ductular proliferation, and liver cirrhosis was examined, and the number of dysplastic cells were evaluated, emphasizing especially on the difference among the several groups. Rats were administered 300mg/kg or 600mg/kg of chloroform(CHCl_(3)-corn oil 1:4 solution) intraperitoneally, and then twice injected weekly for 36 weeks. The control animals were given as similar volume of saline or corn oil, respectively. The animals were sacrificed in 3rd, 6th and 9th month after chloroform injection. The histopathologic changes in the liver of the control and experimenal groups were noted as follows: 1) The hyperplastic nodules in the 600 mg/kg chloroform treated group were more prominent than those of the 300 mg/kg chloroform treated group in the number and size. 2) The number of dysplastic hepatocytes were increased gradually as the experiment continiued. The incidence of dysplastic hepatocytes was 45.5% in the 300 mg/kg treated group and 70.6% in the 600 mg/kg treated group. 3) Oval cells appeared in the early days of the experiment (3rd month) and then gradually decreased in number. 4) The degree of severity of liver cirrhosis and bile duct or ductular proliferation gradually increased as the experiment continued. Incidence of liver cirrhosis and bile duct or ductular proliferation was 31.8% in the 300 mg/kg treated group and 64.7% in the 600 mg/kg treated group, respectivley. 5) Incidence of the chloroform induced hepatoma was 5.9%(1 out of 17 rats) in the chloroform 600 mg/kg treated group, and the hepatoma spread to the liver, followed by metastasis to the omentum and ileum. 6) Light microscopically, some hepatic lobules revealed some foci of vacuolated or clear hepatocytes. Electron microscopically, they contained fat droplets. Others also contained increased number of mitochondria or distorted mitochondria. In summary, the result obtained by the present study indicates chloroform induced hyperplastic nodules, liver cell dysplasia, oval cell proliferation and liver cirrhosis, and secondarily induced hepatoma.
Sumoylation of histone deacetylase 1 regulates MyoD signaling during myogenesis
정호석,권세희,김경훈,이윤경,신세라,권덕화,이영운,국태원,최낙원,김정철,김영국,엄광현,국현 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-
Sumoylation, the conjugation of a small ubiquitin-like modifier (SUMO) protein to a target, has diverse cellular effects. However, the functional roles of the SUMO modification during myogenesis have not been fully elucidated. Here, we report that basal sumoylation of histone deacetylase 1 (HDAC1) enhances the deacetylation of MyoD in undifferentiated myoblasts, whereas further sumoylation of HDAC1 contributes to switching its binding partners from MyoD to Rb to induce myocyte differentiation. Differentiation in C2C12 skeletal myoblasts induced new immunoblot bands above HDAC1 that were gradually enhanced during differentiation. Using SUMO inhibitors and sumoylation assays, we showed that the upper band was caused by sumoylation of HDAC1 during differentiation. Basal deacetylase activity was not altered in the SUMO modification-resistant mutant HDAC1 K444/476R (HDAC1 2R). Either differentiation or transfection of SUMO1 increased HDAC1 activity that was attenuated in HDAC1 2R. Furthermore, HDAC1 2R failed to deacetylate MyoD. Binding of HDAC1 to MyoD was attenuated by K444/476R. Binding of HDAC1 to MyoD was gradually reduced after 2 days of differentiation. Transfection of SUMO1 induced dissociation of HDAC1 from MyoD but potentiated its binding to Rb. SUMO1 transfection further attenuated HDAC1-induced inhibition of muscle creatine kinase luciferase activity that was reversed in HDAC1 2R. HDAC1 2R failed to inhibit myogenesis and muscle gene expression. In conclusion, HDAC1 sumoylation plays a dual role in MyoD signaling: enhancement of HDAC1 deacetylation of MyoD in the basally sumoylated state of undifferentiated myoblasts and dissociation of HDAC1 from MyoD during myogenesis.
대돈(大敦) 보(補) 음곡(陰谷) 사(瀉) 자침(刺鍼)이 정상 흰쥐의 뇌혈류력학(腦血流力學) 변화(變化)에 미치는 영향(影響)
정호석,류충열,조명래,Jung, Ho-Suk,Ryu, Chung-Ryeol,Cho, Myung-Rae 대한침구의학회 2009 대한침구의학회지 Vol.26 No.2
Objectives: The purpose of this study is to investigate the effects of Daedon($LR_1$) Supplementation and Eumgok($KI_{10}$) Draining on changes of cerebral blood flow in normal rats. Methods : Regional cerebral blood flow(rCBF) and mean arterial blood pressure(MABP) in normal rats are observed, and those mechanisms were also investigated with pre-treatment of indomethacin (IDM) and methylene blue(MTB) each. Results : In this study, $LR_1$ supplementation and $KI_{10}$ draining elevated level of rCBF after 30 min, but MABP level was lowered at 30 min, then recovered toward normal level. Pre-treatment with indomethacin (IDM), an inhibitor of cyclooxygenase, inhibited increase of rCBF effectively, and pre-treatment with methylene blue(MTB), an inhibitor of guanylate cyclase, also inhibited increase of rCBF levels. On the other hand pre-treatment with IDM or MTB did not affect MABP levels. Conclusions : In conclusion, these results suggest that $LR_1$ supplementation and $KI_{10}$ draining can increase rCBF, and the mechanisms are thought to be related to both of cyclooxygenase and Guanylate cyclase pathways.