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아세트아미노펜에 의해 간손상이 유발된 랫드의 유전자 발현 분석
정희경(Heekyoung Chung) 한국독성학회 2006 Toxicological Research Vol.22 No.4
Global gene expression profile was analyzed by microarray analysis of rat liver RNA after acute acetaminophen (APAP) administration. A single dose of 1 g/㎏ body weight of APAP was given orally, and the liver samples were obtained after 24, 48 h, and 2 weeks. Histopathologic and biochemical studies enabled the classification of the APAP effect into injury (24 and 48 h) and regeneration (2 weeks) stages. The expression levels of 4900 clones on a custom rat gene microarray were analyzed and 484 clones were differentially expressed with more than a 1.625-fold difference (which equals 0.7 in log2 scale) at one or more time points. Two hundred ninety seven clones were classified as injury-specific clones, while 149 clones as regeneration-specific ones. Characteristic gene expression profiles could be associated with APAP-induced gene expression changes in lipid metabolism, stress response, and protein metabolism. We established a global gene expression profile utilizing microarray analysis in rat liver upon acute APAP administration with a full chronological profile that not only covers injury stage but also later point of regeneration stage.
페닐부타존에 의해 간손상이 유발된 생쥐의 유전자 발현 분석
이은주(Eun-Ju Lee),정인해(In-Hye Jeong),김한나(Han-Na Kim),정희경(Heekyoung Chung),공구(Gu Kong),강경선(Kyung-Sun Kang),윤병일(Byung-IL Yoon),이병훈(Byeong Hoon Lee),이미옥(Mi-Ock Lee),김주한(Ju Han Kim),김형래(Hyung-Lae Kim) 한국독성학회 2006 Toxicological Research Vol.22 No.2
The KFDA (Korea Food & Drug Administration) has performed a collaborative toxicogenomics project since 2003. Its aim is to construct a toxicologenomic database of 12 hepatotoxic compounds from mice livers. Phenylbutazone which is non-steroidal anti-inflammatory drug was assigned. It was administered at low (0.0238 ㎎/㎏) and at high (0.238 ㎎/㎏) dose (5 mice per group) orally to the postnatal 6 weeks ICR mice, then the serum and liver were collected at the indicated time (6, 24 and 72 h) after administration. Serum biochemical markers for liver toxicity were measured and histopathologic studies also were carried out. The gene expression profiling was carried out by using Applied Biosystems 1700 Full Genome Expression Mouse. The 2-way ANOVA was used to find genes that reflected phenylbutazone-induced acute toxicity or dose-dependant changes. By self-organization maps (SOM), we identified groups with unique gene expression patterns, some of them are supposed to be related to phenylbutazone induced toxicity, including lipid metabolism abnormality, oxidative stress, cell death and cytoskeleton destruction.