D-갈락토사민/Lipo다당류로 인한 급성 간 손상에 대한 코디세핀의 보호 효과

한국어 요약

2017년 발표된 「The Protective Effect of Cordycepin on D-Galactosamine/Lipopolysaccharide-Induced Acute Liver Injury」은(는) Cordyceps militaris (동충하초) 및 코디세핀 관련 동물·세포 실험(전임상)입니다. 아래는 원문 초록을 바탕으로 한 중립적 요약이며, 제품 효능·효과를 의미하지 않습니다.

초록 요지

As the major active ingredient of Cordyceps militaris , cordycepin (3′-deoxyadenosine) has been well documented to alleviate inflammation and oxidative stress both in vitro and in vivo. To explore the potential protective effect of cordycepin in fulminant hepatic failure, mice were pretreated with cordycepin for 3 weeks followed by D-galactosamine (GalN)/lipopolysaccharide (LPS) injection. Then we found cordycepin (200 mg/kg) administration elevated survival rate, improved liver function, and suppressed hepatocyte apoptosis and necrosis in mice with severe hepatic damage by GalN/LPS treatment. Further, cordycepin inhibited hepatic neutrophil and macrophage infiltration and prevented proinflammatory cytokine production possibly through suppressing TLR4 and NF- κ B signaling transduction. The blockade of reactive oxygen species (ROS) and lipid peroxidation production by cordycepin was associated with the decrease of NAD(P)H oxidase (NOX) activity. Besides, cordycepin significantly prevented excessive autophagy induced by GalN/LPS in the liver. These data suggested that cordycepin could be a promising therapeutic agent for GalN/LPS-induced hepatotoxicity.

전문가 메모

• 연구 수준: 동물/세포 실험 · 동물·세포 실험(전임상)
• 대상: Cordyceps militaris (동충하초) / cordycepin
• 제품 연관성: direct
• 해석 주의: 전임상(동물·세포) 결과는 인간 섭취·담금주 맥락으로 직접 확장하기 어렵습니다.
• 해석 주의: 원문에 질병·치료 관련 서술이 포함되어 있습니다. 본 요약은 성분·균류 연구 맥락만 중립적으로 정리했습니다.
• 인사이트: 배양·생산·기초 메커니즘 연구로 읽는 것이 적절합니다. 소비자 효능 주장 근거로 사용할 수 없습니다.

출처 · 원문

• 제목: The Protective Effect of Cordycepin on D-Galactosamine/Lipopolysaccharide-Induced Acute Liver Injury
• 저자: Jin Li 외 3명
• 연도: 2017
• 저널: Mediators of Inflammation
• DOI: 10.1155/2017/3946706
• PMID: 28522898
• 링크: https://doi.org/10.1155/2017/3946706

원문 초록 (English)

Summary — As the major active ingredient of Cordyceps militaris , cordycepin (3′-deoxyadenosine) has been well documented to alleviate inflammation and oxidative stress both in vitro and in vivo. To explore the potential protective effect of cordycepin in fulminant hepatic failure, mice were pretreated with cordycepin for 3 weeks followed by D-galactosamine (GalN)/lipopolysaccharide (LPS) injection. Then we found cordycepin (200 mg/kg) administration elevated survival rate, improved liver function, and suppressed hepatocyte apoptosis and necrosis in mice with severe hepatic damage by GalN/LPS treatment. Further, cordycepin inhibited hepatic neutrophil and macrophage infiltration and prevented proinflammatory cytokine production possibly through suppressing TLR4 and NF- κ B signaling transduction. The blockade of reactive oxygen species (ROS) and lipid peroxidation production by cordycepin was associated with the decrease of NAD(P)H oxidase (NOX) activity. Besides, cordycepin significantly prevented excessive autophagy induced by GalN/LPS in the liver. These data suggested that cordycepin could be a promising therapeutic agent for GalN/LPS-induced hepatotoxicity.

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