• 한국식품과학회지
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• 제52권5호
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• pp.476-481
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• 2020

본 연구에서는 간보호 활성이 우수한 것으로 알려진 단풍취의 활용가치를 높이고 향후 건강기능성식품 소재로써의 가능성을 알아보고자 LPS/D-GalN 독성유발에 따른 단풍취 열수 추출물의 간기능 개선효과를 연구하였다. 단풍취 열수 추출물 내에 존재하는 5종의 Caffeoylquinic acid (CQA) 분석결과 4,5-di-O-caffeoylquinic acid (4,5-DCQA) 11.16 mg/g, 3,4-di-O-caffeoylquinic acid (3,4-DCQA) 5.23 mg/g, 5-O-caffeoylquinic acid (5-CQA) 4.88 mg/g, 3,5-di-O-caffeoylquinic acid (3,5-DCQA) 3.51 mg/g 및 4-O-caffeoylquinic acid (4-CQA) 3.31 mg/g 순으로 나타났다. 단풍취 열수 추출물이 함유하고 있는 총 폴리페놀 함량은 74.03 mg/g이었으며, ABTS cation radical 소거능은 추출물의 농도 50, 100, 200 및 400 ㎍/mL의 범위에서 각각 12.2, 25.0, 40.8, 68.55%를 나타냈고 DPPH radical 소거능은 50 ㎍/mL의 농도에서 54.38%를 나타냈다. HepG2 세포에 LPS/D-GalN을 처리하여 간독성을 유발한 결과 정상군을 제외한 모든 처리군에서 GGT, AST 및 LDH 활성이 증가하였고, 단풍취 열수 추출물 300 mg/mL을 처리하였을 때 대조군과 비교하여 GGT, AST 및 LDH 활성이 유의적으로 감소하는 것으로 나타났다. LPS/D-GalN을 처리하였을 때 정상군과 비교하여 모든 처리군에서 TNF-α 분비가 유의적으로 증가하는 것을 확인 할 수 있었으며, 단풍취 열수 추출물을 100 ㎍/mL 이상 처리하였을 때 TNF-α의 분비가 유의하게 감소하였다. 이상의 결과로 볼 때 단풍취 열수 추출물은 항산화 활성 증가 및 GGT, AST, LDH의 활성을 감소시키고 TNF-α 분비를 억제시킴으로써 LPS/D-GalN으로 인한 간 손상을 예방하는 것으로 판단된다.

• IMMUNE NETWORK
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• 제1권3호
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• pp.213-220
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• 2001

Background: A previous study has shown that Euonymus alatus (EA) has an antidotic activities against inflammation, suggesting possibility that EA can exert this beneficial effects to liver injury by an initial protection against drug-induced hepatocyte demage. The present study was undertaken to evaluate the protective effect of EA-extract on experimentally induced hepatitis in ICR mice and to investigate some mechanisms responsible for its action. Methods: Water EA extract was used in this experiments. The mice received i.p. a dose of 700 mg/kg galactosamine (GalN) together with $5{\mu}g/kg$ of endotoxin (LPS), or received i.v. 12 mg/kg of concanavalin A (Con A). EA (4 mg/mouse) was administrated on day -2, -1 and 0 before induction of liver injury. Liver injury was assessed by measurement of serum alanin amino-transferase (SGPT) levels on 9 hr after GaIN.LPS, or 8 hr after con A administration. Results: Treatment with either GaIN or LPS alone did not cause hepatitis. However, simultaneous administration of GalN and LPS to mice resulted in LPS-dose dependent fulminant hepatitis. GaLN/LPS-induced liver injury was reduced when mice were given EA for 3 days before induction. This preventive effect of Ea was more prominent when EA was given by intraperitoneal route rather then by oral route. Pretreatment of EA or dexamethasone inhibited significantly $TNF{\alpha}$ production in GalL/LPS-injured mice. However, EA-treatment did not influence $TNF{\alpha}$-induced hepatitis in GalN-sensitized mice, suggesting that $TNF{\alpha}$ is likely to act as one of final mediators of endotoxin action and the protective effect of EA might be manifested chiefly by inhibition of endotoxin-induced $TNF{\alpha}$ production, not by blocking the $TNF{\alpha}$-action. Injection of Con A into mice evoked remarkable liver injury in a dose dependent fashion. This liver damage was reduced by EA-pretreatment. Dexamethasone significantly reduced both GalL/LPS-induced and Con A-induced liver damages, showing synergism with EA. However, indomethacin reduced only GalN/ LPS-induced hepatitis, not for Con A-induced hepatitis. Conclusion: These results led to the conclusion that EA may be able to contribute at least in part to prevent the drug-induced hepatotoxicity, and that its anti-hepatitis effects might be manifested directly by modulation of endogenous mediators, such as leukotriese D4, $TNF{\alpha}$ and free radical, and indirectly by regulation of immune mediated responses. Also these results suggested that EA could be developed as a potential antidotic agent.