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- 저자 : Jung M. Kweon(권정민) (검색결과 1 건)
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Yeong L. Ha(하영래),Young S. Kim(김영숙),Chae R. Ahn(안채린),Jung M. Kweon(권정민),Cherl W. Park(박철우),Young K. Ha(하영권),Jeong O. Kim(김정옥) 한국생명과학회 2010 생명과학회지 Vol.20 No.1
LED의 간 보호 기능을 연구하기 위하여 CCl₄ 및 ethanol로 SD rat에 간독성을 유발한 다음, LED를 처리하였다. LED의 간 기능 보호효과는 간장치료제인 Silymarin과 비교하였다. CCl₄로 간 독성을 유발한 경우, LED는간의 항산화효소인 SOD, catalase, GSH peroxidase 효소활성의 항진을 유도하였고, 산화물인 TBARS의 함량을 감소시켰다. 또한 간 손상의 지표인 혈장의 GOT, GPT 및 LDH의 활성을 감소시켰다. Ethanol로 간 독성을 유발한 경우 LED는 간의 SOD, catalase, GSH preoxidase 효소활성 및 GSH 함량을 항진시켰고, 총 cholesterol, triglyceride 및 TBARS의 함량을 감소시켰다. 또한 ethanol 대사에 관여하는 ADH 효소 활성을 증진시켰고, ROS 생성에 관여하는 CYP2E1 효소의 발현을 감소시킴으로써, 혈장의 GOT, GPT 및 LDH 효소활성이 감소되었다. 또한 LED는 DPPH 및 mouse liver mitochondrial system에서 항산화효과를 보였다. 이러한 결과로 미루어 볼 때 LED는 in vitro와 in vivo에서 항산화효과에 의한 간 기능 보호효과를 갖는 것으로 추정된다. The protective effect of a mixed powder from solid-cultured and liquid-cultured Lentinus edodes mycelia (2:1, w/w) (designate LED) on the carbon tetrachloride (CCl₄)- and ethanol-induced hepatotoxicity of male Sprague-Dawley (SD) rat was investigated. In the CCl₄-induced rat hepatotoxicity experiment, rats of 4 groups (6 rats/group) were administere with Normal (0.2 ml distilled water), Control (0.2 ml distilled water), LED (LED 200 ㎎/㎏ BW + 0.2 ml distilled water), and Silymarin (200 ㎎/㎏ BW + 0.2 ml distilled water), p.o., daily for 2 weeks. Afterwards, all groups except for the Normal group were subjected to abdominal injection with CCl₄ (CCl₄: corn oil, 1:1 v/v; 0.5 ml/㎏ BW). For the ethanol- induced rat hepatotoxicity experiment, rats were divided into 5 groups (5 rats/group): Normal; Pair-fed control (PFC); Control (ethanol); LED (ethanol + LED 200 ㎎/㎏ BW); and Silymarin (ethanol + silymarin 200 ㎎/㎏ BW). Rats of the Normal and PFC groups were fed a basal liquid diet, and rats of the Control, LED, and Silymarin groups were fed a liquid ethanol diet containing LED or Silymarin. Eight weeks later, blood and liver samples were collected to analyze biomarkers. In CCl₄-induced SD rats, LED elevated hepatic superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH peroxidase) activities and thiobarbituric reactive substances (TBARS) were reduced, resulting in the reduction of glutamate-oxalate transaminase (GOT), glutamate-pyruvate transaminase (GPT) and lactic dehydrogenase (LDH) activities in plasma. Similar results of these enzymes and biochemical markers in both liver tissues and plasma were seen in ethanol-induced hepatotoxicity of SD rats. In addition, elevated alcohol dehydrogenase (ADH) activity and reduced expression of cytochrome p450 mixed monooxygenase enzyme (CYP2E1) were seen in liver tissues from ethanol-treated rats by LED treatment. These effects of LED were similar to those of Silymarin. In in vitro experiments, LED showed antioxidant activity in a 2,2-diphenyl-1-picrylhydrazyl (DPPH) system and mouse liver mitochondria system induced by NADPH/Fe<SUP>2+</SUP> and cumine hydroperoxide (CuOOH). These results indicate that LED protected SD rat hepatotoxicity, induced by CCl₄ and ethanol, through its antioxidative activity and might be useful as a material for protection from hepatoxicity in humans.
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