국내자생 피조개의 암세포 분화유도 및 면역조절 기능 연구

Abstract

The effect of alcohol fraction(SⅢ) prepared from blood shell on cell differentiation was investigated in a HL-60 cell culture system. Treatment of HL-60 cells with 2.5-20 ㎍/㎖ alcohol fraction of blood shell for 72h result in inhibited cell proliferation by the concentration more than 5 ㎍/㎖ and induced increase in cell differentiation. Interestingly, synergistic induction of HL-60 cell differentiation was observed when the alcohol fraction of blood shell was combined with either 5nM 1,25-(OH)2D3 or 50nM all-trans retinoic acid. Flow cytometric analysis indicated that combinations of 1,25-(OH)2D3 and alcohol fraction of blood shell stimulated differentiation predominanatly to monocytes whereas combinations all-trans retinoic acid and the acetone fraction of bamboo leaf stimulated differentiation predominantly to granulocytes. These results suggest that the alcohol fraction of blood shell enhanced leukemia cell differentiation and suggest a possibility of blood shell in the treatment of leukemia. Also, We investigated the effects of ethanol fraction prepared from blood shell on the production of IL-12 from mouse macrophages stimulated with lipopolysaccharide(LPS). Pharmacological inhibition of interleukin-12(Il-12) production may allow a therapeutic strategy for preventing development and progression of disease in experimental models of autoimmunity. The alcohol fraction of blood shell potently inhibited the LPS-induced IL-12 production from RAW 264.7 monocytic cell-line in a dose-dependent manner. The effect of the alcohol fraction of blood shell on IL-12 gene promoter activation was analyzed by transfecting RAW 264.7 cells with IL-12 gene promoter/luciferase constructs. The repressive effect mapped to a region in the IL-12 gene promoter containing a binding site for NF-κB. Futhermore, activation of macrophage by LPS resulted in markedly enhanced binding activity to the NF-κB site, which significantly decreased upon addition of the alcohol fraction of blood shell, indicating that the alcohol fraction of blood shell inhibited IL-12 production in LPS-activated macrophages via inhibition of NF-κB binding activity.