• 제목/요약/키워드: ${\alpha}$-Methyl-n-butylshikonin

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자근으로부터 혈소판에 작용하는 천연색소물질에 관한 연구 (Effects of Shikonin Pigments from the Roots of Lithospermum eryhrorhizon on Rabbit Platelets)

  • 박영현;장성근
    • 한국식품위생안전성학회지
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    • 제15권2호
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    • pp.167-172
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    • 2000
  • 최근 동물성 식품 및 지방 섭취 증가로 인한 현대인의 식생활 변화로 혈소판 활성화가 직접적 원인인 뇌 .심혈관질환의 사망률이 증가되고, 성인병 예방과 치료의 대처방안으로 식품의 기능성에 대한 관심이 높아짐에 따라서 천연착색료이며 항균, 항암 작용이 있는 자근(Lithospermum erythrorhizon)으로부터 추출, 분리 . 정제한 분획물에서 혈소판 활성화 억제작용이 있는 생리활성물질을 분리 . 동정하였다 자근에서 methanol, n-hexane, ethyl acetate 등의 용매추출물과 methanol 추출물에 NaOH프 처리한 n-hexane 추출물에 대한 혈소판 응집 억제작용은 collagen의 응집작용에 대하여 n-hexane재추출물이, thrombin의 응집작용에 대하여 ethyl acetate추출물이 큰 억제작용을 보였고, 이러한 추출물에서 컬림 및 HPLC로 분리 .정제한 5개 물질의 화학구조를 IH과 13C-NMR 스펙트라 분석한 결과 shikonin, acethylshi onin, isobutylshikonin, $\alpha$-methyl-n-butylshikonin, $\beta$,$\beta$-dimethylacrylshikonin을 확인하였고, 혈소판 응집 억제작용은 $\beta$,$\beta$-dimethylacrylshi onin$\geq$$\alpha$-methyl-n-butylshikonin>isobutylshikonin>acetylshikonin>shikonin순으로 나타났다. 이상의 결과로부터 자근색소의 생리활성은 shikonin유도체이며 11번 탄소에 치환된 aliphatic 기의 탄소수가 많을수록 억제작용이 강하게 나타난다고 사료된다.

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Activation of JNK/p38 Pathway is Responsible for α-Methyl-n-butylshikonin Induced Mitochondria-Dependent Apoptosis in SW620 Human Colorectal Cancer Cells

  • Wang, Hai-Bing;Ma, Xiao-Qiong
    • Asian Pacific Journal of Cancer Prevention
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    • 제15권15호
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    • pp.6321-6326
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    • 2014
  • ${\alpha}$-Methyl-n-butylshikonin (MBS), one of the active components in the root extracts of Lithospermum erythrorhizon, posses antitumor activity. In this study, we assess the molecular mechanisms of MBS in causing apoptosis of SW620 cells. MBS reduced the cell viability of SW620 cells in a dose-and time-dependent manner and induced cell apoptosis. Treatment of SW620 cells with MBS down-regulated the expression of Bcl-2 and up-regulated the expression of Bak and caused the loss of mitochondrial membrane potential. Additionally, MBS treatment led to activation of caspase-9, caspase-8 and caspase-3, and cleavage of PARP, which was abolished by pretreatment with the pan-caspase inhibitor Z-VAD-FMK. MBS also induced significant elevation in the phosphorylation of JNK and p38. Pretreatment of SW620 cells with specific inhibitors of JNK (SP600125) and p38 (SB203580) abrogated MBS-induced apoptosis. Our results demonstrated that MBS inhibited growth of colorectal cancer SW620 cells by inducing JNK and p38 signaling pathway, and provided a clue for preclinical and clinical evaluation of MBS for colorectal cancer therapy.