• Korean Journal of Pharmacognosy
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• v.43 no.3
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• pp.231-238
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• 2012

Menthae herba (MH) extracts exhibit anti-inflammatory effects. The purpose of this study was to determine whether the anti-inflammatory effects of MH extracts vary according to the cultivation regions. We performed a comparative analysis of MH extracts by evaluating the production of inflammatory mediators in RAW 264.7 murine macrophage cells and HaCaT human keratinocyte cells. MH extracts obtained from different cultivation regions in Korea and China significantly reduced the production of nitric oxide (NO), prostaglandin $E_2$ ($PGE_2$), and tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) in RAW 264.7 cells stimulated with lipopolysaccharide (LPS). No differences in these inhibitory activities were observed between MH extracts. In HaCaT cells stimulated with TNF-${\alpha}$ and interferon-${\gamma}$ (IFN-${\gamma}$), MH extracts did not inhibit the production of macrophage-derived chemokine (MDC/CCL22), but most extracts reduced the production of the regulated on activation normal T-cell expression and secreted (RANTES/CCL5). We used clustering tree analysis of the MH extracts according to the chromatographic pattern and anti-inflammatory potency of MH extracts. We observed differences in the chromatographic pattern of MH extracts but no difference in anti-inflammatory potency. Our findings suggest that MH extracts from different regions do not show any differences in their pharmacological potency in that MH extracts are used as therapeutic agents to treat inflammatory disorders.

• Biomolecules & Therapeutics
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• v.16 no.4
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• pp.385-393
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• 2008

As an attempt to search for bioactive natural products exerting anti-inflammatory activity, we evaluated the effects of the methanol extract of Polytrichum commune Hedw (PCM) (Polytrichaceae) on lipopolysaccharide (LPS)-induced nitric oxide (NO), prostaglandin $E_2$ ($PGE_2$) and pro-inflammatory cytokines release in murine macrophage cell line RAW 264.7. PCM potently inhibits the production of NO, $PGE_2$, tumor necrosis factor (TNF)-$\alpha$ and interleukin (IL)-6. Consistent with these results, PCM also concentration-dependently inhibited LPS-induced inducible NO synthase (iNOS) and cyclooxygase (COX)-2 at the protein levels, and iNOS, COX-2, TNF-$\alpha$ and IL-6 at the mRNA levels without an appreciable cytotoxic effect on RAW 264.7 macrophag cells. Furthermore, PCM inhibited LPS-induced nuclear factor-kappa B (NF-$\kappa$B) activation as determined by NF-$\kappa$B reporter gene assay, and this inhibition was associated with a decrease in the nuclear translocation of p65 and p50 NF-$\kappa$B. Taken together, these results suggest that PCM may play an anti-inflammatory role in LPS-stimulated RAW 264.7 macrophages through the inhibitory regulation of iNOS, COX-2, TNF-$\alpha$ and IL-6 via NF-$\kappa$B inactivation.

• Korean Journal of Food Science and Technology
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• v.31 no.2
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• pp.535-539
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• 1999

Soybean has drawn much attention mainly due to its chemopreventive action as well as antiestrogenic effect. Although suppression of breast and prostate cancers were believed to be exerted via antiestrogenic or antiandrogenic activity of genistein, its mechanism of prevention against other cancers has not been clearly demonstrated. We proposed that prevention by soybean from other cancers than sex hormone -related cancers was achieved via modulation of drug-metabolizing enzymes. Addition of acid hydrolysate of 80% methanol extract of soyflour to diet caused a significant induction of quinone reductase, an anticarcinogenic marker enzyme and one of drug-metabolizing enzymes, in mouse lung while it suppressed arylhydrocarbon hydroxylase, involved in bioactivation of procarcinogens, in kidney and small intestine. It is likely that active components exist in a conjugated form and released by acid hydrolysis to be able to affect drug-metabolizing enzyme and exert chemopreventive activity. Benzo(a)pyrene-induced tumor development in mouse lung was greatly reduced by soybean extract supplementation, which is consistent with the extract's capability to modulate favorably arylhydrocarbon hydroxylase and quinone reductase towards chemoprevention.

• Bulletin of the Korean Chemical Society
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• v.35 no.10
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• pp.2955-2962
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• 2014

Asian ginseng is used as a treatment for cardiovascular diseases, ischemia, and cancers. High mobility group box 1 (HMGB1) protein acts as a late mediator of severe vascular inflammatory conditions. However, the effect of ginsenosides from Asian ginseng on HMGB1-induced inflammatory responses has not been studied. We addressed this question by monitoring the effects of ginsenoside treatment on lipopolysaccharide (LPS) and cecal ligation and puncture (CLP)-mediated release of HMGB1, and HMGB1-mediated regulation of proinflammatory responses. Ginsenoside treatment suppressed LPS-mediated release of HMGB1 and HMGB1-mediated cytoskeletal rearrangements. Ginsenosides also inhibited HMGB1-mediated inflammatory responses. In addition, ginsenosides inhibited the production of tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and activation of protein kinase B (Akt), nuclear factor-${\kappa}B$ (NF-${\kappa}B$), and extracellular-regulated kinases (ERK) 1/2 by HMGB1. Ginsenosides also decreased CLP-induced release of HMGB1, production of interleukin (IL) $1{\beta}/6$, and mortality. These results suggested that ginsenosides may be potential therapeutic agents for treatment of vascular inflammatory diseases through inhibition of the HMGB1 signaling pathway.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2018.04a
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• pp.91-91
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• 2018

Poncirus Fructus (PF) is obtained by drying the trifoliate orange fruit belonging to the Rutaceae family. In our country of medicine, PF has been used as a treatment of indigestion, allergy and inflammation. But Mechanism and medical data for PF is insignificant. Recently, the effect of the study PF of biological activity was reported, such as anti- thrombosis, anti-bacteria, anti-virus, anti- allergic. We investigated that the effect of PF on anti-inflammatory in murine macrophage-like cell line Raw264.7 cells. Our results show that the expression level of Nitric Oxide (NO) and Matrix-metallopeptidase-9 (MMP-9) significantly decreased. Moreover, to determine the expression level of pro-inflammatory cytokines such as Tumor Necrosis Factor ($TNF-{\alpha}$) and Interleukin-6 (IL-6) and the phosphorylation pattern of signaling molecules of mitogen-activated protein kinase (MAPK) family, we performed ELISA and westren blot in Raw264.7 cells. In addition, nuclear factor-kappa B ($NF-{\kappa}B$) pathway was confirmed. PF extract inhibited the production of $TNF-{\alpha}$ and IL-6. The extract suppressed the phosphorylation of ERK1/2, JNK, and p38 MAPK, and the nuclear translocation of $NF-{\kappa}B$ p65 in activated cells. Our results suggest that PF can be used as a potential therapeutic agent or functional food to relieve inflammation.

• Mycobiology
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• v.43 no.4
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• pp.450-457
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• 2015

Medicinal mushrooms have been used worldwide to treat cancer and modulate the immune system. Over the last several years, there has been increasing interest in isolating bioactive compounds from medicinal mushrooms and evaluating their health beneficial effects. Fomes fomentarius is used in traditional oriental medicine and is known to possess antioxidant, antiinflammatory, antidiabetic, and antitumor effects. In the present study, we isolated fomentariol from Fomes fomentarius and investigated its anti-inflammatory effect in murine macrophages (RAW264.7 cells) stimulated with lipopolysaccharides. Fomentariol inhibited the production of nitric oxide and intracellular reactive oxygen species triggered by lipopolysaccharides. Interestingly, fomentariol differentially regulated cytokine production triggered by lipopolysaccharides. Fomentariol effectively suppressed the production of interleukin-$1{\beta}$ and interleukin-6 but not tumor necrosis factor-${\alpha}$. The inhibitory effect of fomentariol against nitric oxide, interleukin-$1{\beta}$, and interleukin-6 production was possibly mediated by downregulation of the extracellular signal-regulated kinase signaling pathway. Taken together, our results suggest that fomentariol differentially modulated inflammatory responses triggered by lipopolysaccharides in macrophages and is one of the bioactive compounds that mediate the physiological effects of Fomes fomentarius.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.11 no.1
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• pp.1-22
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• 1998

During the last few years, nitric oxide(NO) as a potent macrophage-derived effector molecule against a variety of bacteria, parasites, and tumors has received increasing attention. More recent studies suggest that NO also has antiviral effects in both murine and human cells. The objective of the current study was to determine the effect of Yongdamsagantang(YST) on the production of NO. Stimulation of mouse peritoneal macrophages with YST after the treatment of recombinant $interferon-{\gammer}(rlFN-{\gammer})$ resulted in the increased NO synthesis. YST had no effect on NO synthesis by itself. When YST was used in combination with $rIFN-{\gammer}$, there was a marked cooperative induction of NO synthesis in a dose-dependent manner. The optimal effect of YST on NO synthesis was shown 6 hour after treatment with $rIFN-{\gammer}$. This increase in NO synthesis was reflected as increased amount of inducible NO synthase(iNOS) protein. NO production was inhibited by $N^G-monomethyl-L-arginine$. The increased production of NO from $rIFN-{\gammer}$ plus YST-stimulated cells was decreased by the treatment with staurosporin. In addition, synergy between $rIFN-{\gammer}$ and YST was mainly dependent on YST-induced tumor necrosis $factor-{\alpha}(TNF-{\alpha})$ secretion. These results suggest that the capacity of YST to increase NO production from $rIFN-{\alpha}-primed$ mouse peritoneal macrophages is the result of YST-induced $TNF-{\alpha}$ secretion.

• Preventive Nutrition and Food Science
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• v.15 no.3
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• pp.206-212
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• 2010

Codium fragile (CF) is an edible green alga consumed as a traditional food source in Korea. In this study, the ethanol extract of CF was evaluated to determine if it has anti-inflammatory activity. Lipopolysaccharide (LPS), a toxin from bacteria, is a potent inducer of inflammatory cytokines, such as tumor necrosis factor (TNF)-$\alpha$ and interleukin (IL)-6. Therefore, we studied whether CF extracts have an anti-inflammatory effect in LPS-induced murine macrophage cell lines (RAW 264.7). In the present study, IL-6 production was measured using an enzyme-linked immunosorbent assay (ELISA), prostaglandin $E_2$($PGE_2$) production was measured using the EIA kit, and cyclooxygenase (COX)-2 and mitogen-activated protein kinase (MAPK) activation were determined by Western blot analysis. IL-6 mRNA, COX-2 mRNA and iNOS mRNA expression were measured using reverse transcription-polymerase chain reaction (RT-PCR). The results indicated that CF extracts inhibit LPS-induced IL-6, NO and PGE2 production in a dose-dependent manner, as well as expression of iNOS and COX-2. CF extracts significantly inhibited LPS-induced c-Jun N-terminal kinase (JNK) 1/2 phosphorylation. Taken together, these findings may help elucidate the mechanism by which CF modulates RAW 264.7 cell activation under inflammatory conditions.

• Journal of Microbiology and Biotechnology
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• v.26 no.8
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• pp.1367-1374
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• 2016

The present study evaluated the total phenolic and flavonoid contents as well as total antioxidant capacity (TAC) of three cultivars of Actinidia arguta Planch. kiwi berries; cv. Mansoo (Mansoo), cv. Chiak (Chiak), and cv. Haeyeon (Haeyeon). In addition, the anti-inflammatory effects of the three cultivars of kiwi berries were investigated using a lipopolysaccharide (LPS)-stimulated RAW 264.7 murine macrophage cell line. Mansoo had the highest total phenolic content and TAC among the three cultivars, whereas Chiak had the highest total flavonoid content. The total antioxidant capacities of the kiwi berry extracts were more strongly correlated with total phenolic content than with total flavonoid content. The kiwi berry extracts suppressed the secretion of pro-inflammatory cytokines, including interleukin-6 and tumor necrosis factor-α, from LPS-stimulated RAW 264.7 cells. The release of nitrite, an indirect indicator of nitric oxide, was also ameliorated by pre-treatment with the kiwi berry extracts in a dose-dependent manner. Cellular-based measurements of antioxidant capacity exhibited that the kiwi berry extracts had cellular antioxidant capacities. Such cellular antioxidant effects are possibly attributed to their direct antioxidant capacity or to the inhibition of reactive oxygen species generation via anti-inflammatory effects. Our findings suggest that kiwi berries are potential antioxidant and anti-inflammatory agents.

• Environmental Analysis Health and Toxicology
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• v.22 no.3
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• pp.263-269
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• 2007

Chitosan is a depolymerized and partially deacetylated derivative of chitin. We investigated the cytotoxicity of chitosan in cancer cell lines, such as P388, L1210, HCT-15, SK-HepG-1 and mouse splenocytes as a normal cell by MTT assay. To clarify whether chitosan enhances cytotoxicity of anticancer drugs, we also examined the cytotoxicity of combined treatment with chitosan and anticancer drugs, such as cisplatin, mitomycin C, and 5-fluorouracil in cancer cell lines in vitro. Chitosan ($37.5\;{\mu}g/mL,\;75\;{\mu}g/mL,\;112.5\;{\mu}g/mL,\;and\;150\;{\mu}g/mL$) showed concentration-dependent cytotoxicity in the cancer cell lines. In addition, chitosan showed relatively lower cytotoxicity in normal cells than in the cancer cell lines. Particularly, this trend was significant at high doses of chitosan, i.e. $112.5\;{\mu}g/mL,\;and\;150\;{\mu}g/mL$. Thus, these results suggest that chitosan may selectively induce the growth inhibition in cancer cell lines, compared to normal cells. Furthermore. the co-treatment of chitosan and anticancer drugs exhibited an apparant synergistic cytotoxicity in murine lymphoma cell lines, i.e. P388 and L1210 at $37.5\;{\mu}g/mL$ of chitosan rather than at $75\;{\mu}g/mL$ of chitosan, but such phenomenon could not be observed in solid tumor cell lines, i.e. HCT-15 and SK-HepG-1. However, chitosan did'nt reduced the cytotoxicity against normal mouse splenocytes induced by anticancer drugs. Therefore, it is concluded that the combination of chitosan and anticancer drugs might be useful for the cancer chemotherapy.