• 한국식품영양과학회지
• /
• 제26권1호
• /
• pp.25-31
• /
• 1997

갈근(Puerariae radix)을 MeOH 추출물에서 silica gel column chromatography를 이용하여 플라보노이드 화합물인 daidzin 및 puerarin를 분리하여 low density li-poprotein의 산화에 대하여 실험하였다. 이들 플라보노이드중 daidzin의 경우 100$\mu\textrm{g}$/$m\ell$에서 puerarin은 600$\mu\textrm{g}$/$m\ell$의 농도에서 5$\mu$M Cu$^{2+}$ 매개산화 LDL에 대하여 억제 효과가 좋았다. 이때 같은 농도의 diadzin과 puerarin를 첨가한 산화 LDL의 전기영동의 이동거리는 native LDL 보다는 약간 높았으나 oxidized LDL의 대조군 보다는 이동거리가 낮았다. 또 J774 및 macrophages 유도 산화 LDL에 있어서도 100$\mu\textrm{g}$ daidzin과 600$\mu\textrm{g}$/$m\ell$ puerarin을 첨가 하였을 때 억제효과 나타났다. LDL을 5$\mu$M Cu$^{2+}$존재하에서 산화시킬 때 동일 농도의 daidzin과 puerarin 을 첨가하면 conjugated dienes의 생성이 거의 억제되었다.

• 약학회지
• /
• 제55권5호
• /
• pp.404-410
• /
• 2011

This study was to elucidate the anti-inflammatory activities of a methanol extract derived from the fermented bark of Dioscoreae batatas on LPS-induced activation in macrophages. It was fermented with Lactobacillus fermentum and L. plantarum and then analyzed to identify the contents of methanol extract and diosgenin. The fermented product showed 3-fold increase in the extraction yield by methanol, and 1.8-fold increase in diosgenin contents, compared to that from the dried bark of D. batatas. Although the methanol extract from the unfermented D. batatas inhibited lipopolysaccharide (LPS)-induced production of nitric oxide (NO) and TNF-${\alpha}$ in J774 A.1 cells, the methanol extract from the fermented product revealed significantly the enhanced the inhibitory activities on LPS-induced production of NO and TNF-${\alpha}$. Taken together, our results indicate that fermentation of bark of D. batatas elevates the functional activity inhibiting macrophage activation through the increase of the content of anti-inflammatory compounds. Thus, its methanol extract may be useful as a functional material for the therapy of inflammatory diseases.

• 생약학회지
• /
• 제27권2호
• /
• pp.101-104
• /
• 1996

Hydrogen peroxide is one of major chemicals mediating antitumor and antimicrobial activities of macrophages. We searched natural products enhancing hydrogen peroxide generation from murine macrophage-like cell line J774. Among 21 methanol extracts of Korean medicinal plants, the extract from Cornus officinalis was the most effective. The active component from the fractions was searched by activity guided fractionation, and identified as ursolic acid by spectral data.

• IMMUNE NETWORK
• /
• 제21권5호
• /
• pp.36.1-36.16
• /
• 2021

Peroxiredoxins (Prxs) are ubiquitously expressed peroxidases that reduce hydrogen peroxide or alkyl peroxide production in cells. Prxs are released from cells in response to various stress conditions, and they function as damage-associated molecular pattern molecules. However, the secretory mechanism of Prxs and their roles have not been elucidated. Thus, we aimed to determine whether inflammasome activation is a secretory mechanism of Prxs and subsequently identify the effect of the secreted Prxs on activation of the classical complement pathway. Using J774A.1, a murine macrophage cell line, we demonstrated that NLRP3 inflammasome activation induces Prx1, Prx2, Prx5, and Prx6 secretion in a caspase-1 dependent manner. Using HEK293T cells with a transfection system, we revealed that the release of Prx1 and Prx2 relies on gasdermin-D (GSDMD)-mediated secretion. Next, we confirmed the binding of both Prx1 and Prx2 to C1q; however, only Prx2 could induce the C1q-mediated classical complement pathway activation. Collectively, our results suggest that inflammasome activation is a secretory mechanism of Prxs and that GSDMD is a mediator of their secretion. Moreover, secreted Prx1 and Prx2 bind with C1q, but only Prx2 mediates the classical complement pathway activation.

• BMB Reports
• /
• 제31권6호
• /
• pp.565-571
• /
• 1998

The expression of the endogenous human apolipoprotein(apo)E gene was significantly induced when HepG2 cells were treated with exogenous 25-hydroxy-cholesterol. This sterol-mediated apoE gene upregulation appears to require the participation of a positive element for the apoE gene transcription (PET) ( -169/ -140), a core sequence of upstream regulatory element (URE)1 enhancer of the human apoE gene. This PET was renamed as sterol regulatory element (SRE)4 based on its new role as a sensor for the level of intracellular sterol. Furthermore, a gel mobility shift analysis showed that binding activity of the SRE4 binding protein (BP) obtained from HepG2 cells was induced by sterol treatment, while that from either MCF7 or BT20 cells remained unchanged. Binding activity of SRE4BP was also induced in mouse macrophage cells, J774A.1, by sterol treatment, but it was drastically reduced when cells were subjected to treatment of AY-9944, a potent inhibitor for sterol synthesis. However, binding activity of Spl, which is a co-binding protein to the SRE4 region, remained the same in either condition, suggesting that SRE4BP (formally known as PETBP) may be mainly responsible for the sterol-mediated regulation of the apoE gene expression. Deletion analysis of the core binding site of SRE4BP by gel mobility shift assays showed that the minimal sequence of the SRE4BP binding appears to reside between -157 and -140, confirming the identity of SRE4 with the previously determined core sequence of URE1.

• 생명과학회지
• /
• 제12권3호
• /
• pp.325-331
• /
• 2002

달맞이꽃 추출물로써 항산화활성을 알아보기 위하여 사람 low densty lipoprotein(LDL)에 대하여 실험하였다. 사람 LDL에 CuSO$_4$를 첨가한 후 배양하면서 달맞이꽃 추출을 일정 농도씩 증가시키면서 첨가하여 배양하였다. 달맞이꽃 추출물로서 LDL의 산화에 대한 개시와 연쇄 반응에서 thiobarbituric acid reactivy substances (TBARS)와 전기 영동 및 공액 2중 결합으로 측정하였다. 달맞이꽃 추출물을 LDL에 첨가한 후 macrophage J774로써 배양한 결과 TBARS값은 용량 의존형의 항산화 활성을 나타내었으며 전기 영동 이동상에서도 대조구에 비하여 각 시험구에서 LDL의 산화를 억제하였다. 또 공액 2중 결합에 대한 실험에서 용량 의존형산화 억제 효과를 나타내었다. 달맞이꽃 추출물의 항산화 활성은 40 $\mu\textrm{g}$/ml의 농도에서도 항산화 효과가 있었으나 80$\mu\textrm{g}$/mL의 농도에서는 거의 완전한 억제효과가 있었다. 그리고 비타민 C 및 $\alpha$-dl-tocopherol과 비교한 결과 달맞이들 추출물이 약간 높은 항산화 활성을 나타내었다.

• Parasites, Hosts and Diseases
• /
• 제59권6호
• /
• pp.557-564
• /
• 2021

Macrophages play a key role in chronic inflammation, and are the most abundant immune cells in the tumor microenvironment. We investigated whether an interaction between inflamed prostate cancer cells stimulated with Trichomonas vaginalis and macrophages stimulates the proliferation of the cancer cells. Conditioned medium was prepared from T. vaginalis-infected (TCM) and uninfected (CM) mouse prostate cancer (PCa) cell line (TRAMP-C2 cells). Thereafter conditioned medium was prepared from macrophages (J774A.1 cell line) after incubation with CM (MCM) or TCM (MTCM). When TRAMP-C2 cells were stimulated with T. vaginalis, protein and mRNA levels of CXCL1 and CCL2 increased, and migration of macrophages toward TCM was more extensive than towards CM. Macrophages stimulated with TCM produced higher levels of CCL2, IL-6, TNF-α, their mRNAs than macrophages stimulated with CM. MTCM stimulated the proliferation and invasiveness of TRAMP-C2 cells as well as the expression of cytokine receptors (CCR2, GP130, CXCR2). Importantly, blocking of each cytokine receptors with anti-cytokine receptor antibody significantly reduced the proliferation and invasiveness of TRAMP-C2 cells. We conclude that inflammatory mediators released by TRAMP-C2 cells in response to infection by T. vaginalis stimulate the migration and activation of macrophages and the activated macrophages stimulate the proliferation and invasiveness of the TRAMP-C2 cells via cytokine-cytokine receptor binding. Our results therefore suggested that macrophages contribute to the exacerbation of PCa due to inflammation of prostate cancer cells reacted with T. vaginalis.