Protective Effects of Angelica keiskei Extracts Against D-Galactosamine (GalN)-induced Hepatotoxicity in Rats

  • Choi, Sang-Hoon (Department of Aquatic Life Medicine, College of Ocean Science & Technology, Kunsan National University) ;
  • Park, Kwan-Ha (Department of Aquatic Life Medicine, College of Ocean Science & Technology, Kunsan National University)
  • 투고 : 2011.05.20
  • 심사 : 2011.06.17
  • 발행 : 2011.09.30

초록

아직 분명히 규명되지 않은 부분이 많지만, 신선초가 다양한 측면에서 건강증진 효과가 있다고 믿어져 왔고 따라서 일반인들이 지금까지 사용해 오고 있다. 이 연구에서는 신선초의 메타놀 추출물을 투여한 후, 전형적인 간독성 유발물질인 갈락토사민과 사염화탄소를 투여한 랫드에서 일반적 간독성지표와 지질대사능 지표를 측정함으로써 간장 보호작용이 있는지 시험하였다. 신선초를 독성유발전 7일간 매일 1회씩 200 및 500mg/kg의 용량으로 경구투여 하고, 간독성물질을 복강내로 투여 한 후 독성유발 24시간에 혈장과 간장조직에 대한 분석을 수행하였다. 시험한 두 용량(200 및 500 mg/kg)은 갈락토사민에 의해 유발된 지질과 산화물 증가, 혈장 AST 및 ALT 활성의 증가를 감소시켰다. 또한 신선초 500mg/kg은 갈락토사민이 유발한 혈장 중성지질, 총 콜레스테롤 및 저밀도지단백 콜레스테롤의 농도 증가현상을 감소시켰다. 갈락토사민에 의해 유발된 독성에 대한 효과와는 달리, 사염화탄소로 유발된 AST, ALT 및 과산화지질의 증가현상이 신선초 전투여에 의해 더욱 증가하였다. 이 결과는 갈락토사민에 의한 독성을 신선초 전투여가 감소시킬 수 있지만, 반대로 사염화탄소 유발 독성은 더 악화시킴을 의미한다. 신선초의 사염화탄소 유발 간독성 증강효과에 대한 기전을 이해하기 위해 신선초를 투여한 랫드의 간장내 aninline hydroxyiase의 활성을 측정하였다. 그 결과 사염화탄소가 간독성을 발휘하는 데에 필요한 조건인 대사체로의 변환을 매개하는 이 효소의 간장내 활성이 증가함을 관찰하였다. 종합적으로 신선초가 간장보호효과를 발휘하지만 간독성이 어떤 독소에 의해 유발되었느냐에 따라 향상 보호효과가 있지는 않음을 의미한다.

Although the vegetable Angelica keiskei (AK) has widely been utilized for the purpose of general health improvement among Korean population, its functionalities are not very well defined. In this study, we examined the effects of methanol extract of AK in rats on the biochemical changes induced by two hepatotoxins, D-galactosamine (GalN) and carbon tetrachloride ($CCl_4$). AK was orally administered once daily for 7 days to male rats at 200 and 500 mg/kg, before hepatotoxins. Effects of AK were assessed 24 hr later. AK pretreatments at 200 and 500 mg/kg significantly blunted GalN-induced elevation in liver lipid peroxidation, plasma aspartate-transaminase (AST) and alanine-transaminase (ALT) activities. AK also prevented, after 500 mg/kg but not after 200 mg/kg, the GalN-induced elevation in triglyceride, total cholesterol and LDL-cholesterol levels. Differently from against GalN-induced toxicity, AK did further elevate the $CCl_4$-induced rise in AST, ALT and lipid peroxidation. These results suggest that AK, when pre-administered prior to GalN, exerted protective effects against GalN-induced hepatotoxicity, in contrast however, AK exacerbated that induced by $CCl_4$. To explore possible mechanism for the toxicity-potentiating effects of AK on $CCl_4$, the activity of hepatic drug metabolism after AK treatment was assessed. It was observed that AK increased the activity of aniline hydroxaylase, a cytochrome P450 isoenzyme responsible for metabolic activation of $CCl_4$. This finding suggests that hepatoprotective effects of AK are not equally expected depending on hepatotoxins employed.

키워드

참고문헌

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