• Journal of the Korean Society of Food Science and Nutrition
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• v.26 no.1
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• pp.25-31
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• 1997

Antioxidative activity of daidzin and puerarin isolated from Puerariae radix against oxidation of low density lipoprotein(LDL) was investigated. The concentration of daidzin at 100$\mu\textrm{g}$/$m\ell$ and puerarin at 60$\mu\textrm{g}$/$m\ell$ inhibited Cu$^{2+}$-mediated oxidation of LDL almost completely. The electrophoretic mobility of oxidized LDL by addition of daidzin(100$\mu\textrm{g}$/$m\ell$) and puerarin(60$\mu\textrm{g}$/$m\ell$) was faster than that of native LDL, but slower than that of oxidized LDL. The oxidized LDL induced by J774 or macrophage was inhibited strongly in the presence of 100$\mu\textrm{g}$/$m\ell$ daidzin and 60$\mu\textrm{g}$/$m\ell$ Puerarin. The formation of conjugated dienes in the oxidized LDL was strongly inhibited by 100$\mu\textrm{g}$/$m\ell$ daidzin and 60$\mu\textrm{g}$/$m\ell$ puerarin.n.

• YAKHAK HOEJI
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• v.55 no.5
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• pp.404-410
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• 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.

• Korean Journal of Pharmacognosy
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• v.27 no.2
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• pp.101-104
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• 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
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• v.21 no.5
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• pp.36.1-36.16
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• 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
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• v.31 no.6
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• pp.565-571
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• 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.

• Journal of Life Science
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• v.12 no.3
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• pp.325-331
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• 2002

There is growing interest ill understanding the role and mechanisms of flavonoid as antioxidant on LDL. The antioxidative activity of flavonoid typically present in Oenothers odorate Jacquin was investigated in vitro using a human LDL oxidation assay. In present work, LDL was incubated with increasing concentrations of extracts of extracts of Oenothers odorate Jacquin and LDL oxidation was started by adding CuSO$_4$to the media. Substances in leaves extracts of Oenothers odorate Jacquin are capable of inhibiting the initiation and the propagation of LDL oxidation. They inhibit LDL oxidation, monitored by thiobarbituric acid-reactive substances(TBARS), as well as modification as shown through direct measurement of electrophoretic mobility, diene conjugates. Inhibition is a dose dependent effect that becomes already apparent at concentration of extracts as low as 40$\mu\textrm{g}$/mL. Inhibition is almost complete at 80$\mu\textrm{g}$/mL. Extracts of Oenothers odorate Jacquin were more potent antioxidative activity than either ascorbic acid and dl-a -tocopherol.

• Parasites, Hosts and Diseases
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• v.59 no.6
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• pp.557-564
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• 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.