• Natural Product Sciences
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• v.20 no.2
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• pp.113-118
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• 2014

Ribes fasciculatum which belongs to Saxifragaceae has been widely used as a traditional medicine for the treatment of symptoms associated with lacquer poison. However, pharmacological studies on the R. fasciculatum are extremely limited until now. Thus, in this study, we evaluated the possible anti-inflammatory effects of ethyl acetate fraction of R. fasciculatum (ERF) using IFN-${\gamma}$/LPS-stimulated peritoneal macrophage model. We investigated the change in nitrite level in the absence or presence of ERF after LPS stimulation, and we found that ERF effectively attenuates the NO production in a dose dependent manner without notable toxicity. To determine the mechanism of the inhibitory action of ERF on NO production, we performed iNOS enzyme activity assay and Western blotting. Here we showed that both of iNOS enzyme activities and iNOS expressions were significantly down-regulated by ERF, indicating that these dual activities of ERF are responsible for ERF-mediated NO suppression. In addition, ERF inhibitied the expression of cyclooxygenase-2 (COX-2), an another key enzyme in inflammation through suppression of NF-${\kappa}B$ activation. We also tested anti-inflammatory properties of ERF not only in vitro, but in vivo using trypsin-induced paw edema model in mice. Our results revealed that the increased paw volume in response to trypsin injection was recovered by ERF supplement dose dependently.

• Korean Journal of Pharmacognosy
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• v.39 no.2
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• pp.104-109
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• 2008

We previously reported that anti-inflammatory properties of poncirin, isolated from fruit of Poncirus trifoliata, might be the result from the inhibition of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis $factor-{\acute{a}}$ ($TNF-{\alpha}$) and interlukin-6 (IL-6) expression via the down-regulation of $NF{-\kappa}B$ binding activity. In this study, we investigated whether poncirin has an inhibitory effect on the production of pro-inflammatory mediators ex vivo and whether poncirin could relieve the symptoms of dextran sulfate sodium (DSS)-induced colitis in mice model of inflammatory bowel disease. Poncirin significantly inhibited the productions of NO, IL-6 and $TNF-{\alpha}$ in lipopolysaccharide (LPS)-induced mouse peritoneal macrophage. In addition, poncirin-treated mice when compared to control mice not receiving treatment recovered better from the weight loss caused by DSS-induced colitis. Changes in disease activity index (DAI) of poncirin-treated mice were also more favorable than for control mice and were comparable with mice treated with a typical anti-inflammatory-drug, 5-aminosalichylic acid (5-ASA). In addition, suppression of plasma NO and IL-6 productions of poncirin-treated mice was also observed in DSS-induced colitis. These results suggest that poncirin has potentially useful anti-inflammatory effects mediated by suppression of inflammatory mediator productions.

• Biomolecules & Therapeutics
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• v.20 no.6
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• pp.499-505
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• 2012

Chemoprevention represents a strategy designed to protect cells or tissues against various carcinogens and carcinogenic metabolites derived from exogenous or endogenous sources. Recent studies indicate that plant-derived triterpenoids, like oleanolic acid, may exert cytoprotective functions via regulation of the activity of different transcription factors. The chemopreventive effects may be mediated through induction of the nuclear factor erythroid 2-related factor 2 (Nrf2) transcription factor. Activation of Nrf2 by triterpenoids induces the expression of phase 2 detoxifying and antioxidant enzymes such as NAD(P)H quinone oxidoreductase 1 (NQO1) and heme oxygenase-1 (HO-1) - proteins which can protect cells or tissues against various toxic metabolites. On the other hand, inhibition of other transcription factors, like NF-${\kappa}B$ leads to the decrease in the pro-inflammatory gene expression. Moreover, the modulation of microRNAs activity may constitute a new mechanism responsible for valuable effects of triterpenoids. Recently, based on the structure of naturally occurring triterpenoids and with involvement of bioinformatics and computational chemistry, many synthetic analogs with improved biological properties have been obtained. Data from in vitro and in vivo experiments strongly suggest synthetic derivatives as promising candidates in the chemopreventive and chemotherapeutic strategies.

• Journal of Korean Medicine Rehabilitation
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• v.30 no.1
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• pp.47-61
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• 2020

Objectives This study is carried out to investigate the effects of Lonicera japonica in wound-induced rats. Methods Rats were divided into 5 groups; normal (Nor), control (Veh), positive comparison (PC), Lonicera japonica 100 mg/kg (LL), Lonicera japonica 200 mg/kg (LH), each n=8. Total polyphenol and flavonoid were quantified. 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2'-azino-bis(3 ethylbenzothiazoline-6-sulfonic acid) (ABTS) free radical scavenging activation were measured. Reactive oxygen species (ROS) was measured in serum. Antioxidant factors and inflammatory factors were measured in skin tissue, and also hydroxyproline content. Skin tissue was analyzed by Hematoxylin & Eosin and Masson's trichrome staining method. Results Total polyphenol and flavonoid were 32.86±0.14 mg/g and 67.17±0.57 mg/g. The IC₅₀ values of DPPH and ABTS free radical scavenging activation were 26.69±1.50 ㎍/mL and 49.33±4.52 ㎍/mL. ROS was significantly lower in LL and LH groups. Nuclear factor-erythroid 2-related factor 2 (Nrf2) was significantly higher in LH group and higher in LL group but not significant. Superoxide dismutase 1 (SOD-1), catalase, and heme oxygenase 1 (HO-1) were significantly higher in LL and LH groups. Nuclear factor kappa-B p65 (NF-κBp65), phosphorylated iκBα (p-iκBα), cyclooxygenase 2 (COX-2), and tumor necrosis factor alpha (TNF-α) were significantly lower in LL and LH groups. Hydroxyproline was significantly higher in LL and LH groups. The histopathologic analysis showed that skin tissue had recovered further more in LL and LH groups than in Veh group. Conclusions These results suggest that Lonicera japonica has the anti-oxidant, anti-inflammatory and healing effects in wound-induced rats.

• YAKHAK HOEJI
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• v.60 no.3
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• pp.101-106
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• 2016

Allylthiopyridazine derivatives were synthesized and evaluated for anti-proliferative activities in the previous study. In this study, selected two allylthiopyridazine derivatives (compound I, 3-heptylamino-6-allylthiopyridazine and compound II, 3-dipentylamino-6-allylthiopyridazine) were assessed for cytotoxicity and chronic proliferation in human colon carcinoma RKO cells. Two derivatives dose-dependently inhibited cell viability and proliferation. To elucidate the anticancer mechanism of two derivatives, we investigated the expression level of apoptosis-related proteins in RKO cells. Compound I induced the activation of JNK and expression of p53 and p21. On the other hand, compound II showed no change of p53 level. Interestingly, compound II inhibited the nuclear translocation of NF-${\kappa}B$. This result suggested that compound II suppressed cell proliferation. These different mechanisms of these compounds might have occurred through different steric conformation.

• Journal of Haehwa Medicine
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• v.15 no.2
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• pp.121-134
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• 2006

This study saw the anti-allergy effect by the immunity regulation action of Yanghyelyoonbotang (YHYBT) consists 12 kinds of herbal medicine agents. Consequently, YHYBT controlled the amount of secretion of various infla- mmatory cytokines, chemokine, monocyte chemotactic protein and histamine from cells (HMC-1, THP-1, EoL-1) stimulated by PMA, A23187 or HDM. 1. YHYBT did not show cytotoxicity on cultured human fibroblast cells under 250 ${\mu}g/m\ell$ concentration. 2. YHYBT suppressed IL-8, TNF-$\alpha$, IL-6 mRNA expression in the HMC-1 cell stimulated with PMA and A23187. 3. YHYBT significantly suppressed IL-6 release in the THP-1 and EoL-1 cell stimulated with HDM. 4. YHYBT significantly suppressed histamine release in the HMC-1 cell stimulated with PMA and A23187 in a dose-dependent. 5. YHYBT significantly suppressed $\beta$-Hexosaminidase release in the HMC-1 cell stimulated with A23187 in a dose-dependent. 6. YHYBT suppressed NF-$\kappa$B gene expression in the RBL-2H3 cell stimulated with PMA in a dose-dependent. These results suggested that YHYBT has suppressive effects on allergic reaction and pro-inflammatory cytokines in various cell lines through the regulation of immune system. YHYBT has potential to use as an antiallergic agents.

• Journal of Haehwa Medicine
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• v.15 no.2
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• pp.135-148
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• 2006

Sophorae Radix (SFR) is known as a therapeutic drug that has been used in Oriental traditional medicine for the treatment of skin and mucosal ulcers, gastrointestinal hemorrhage, diarrhea, inflammation and arrhythmia. In the present study, we examined the effects of the aqueous extract of SFR on anti-inflammation, anti-allergic and anti-oxidant effect in various cell lines; they include mouse lung fibroblast cells (hFCs), human mast cells (HMC-1), human monocytic cells (THP-1), and RAW 264.7 cells. Treatment with SFR extract at a concentration of 250 ${\mu}g$/ml for 24h showed no significant decrease in the survival rate of the hFCs. SFR decreased the mRNA expression of IL-8, TNF-$\alpha$, and IL-6 in HMC-1 cells. SFR extract treatment significantly inhi-bited the protein expression of IL-6 and, IL-8 induced by mite in THP-1 cells and it also did MCP-1 expression. We examined the alternation of histamine release in HMC-1 cells for investigating anti-allergic effect of SFR. Histamine secretion decreased after the treatment with SFR. In addition, SFR extract treatment at a concentration of 10 ${\mu}g$/ml, 100 ${\mu}g$ /ml, and 200 ${\mu}g$/ml lowered the $\beta$-hexosaminidase to 10.3%, 21.7%, and 50.8%, respectively. IC50 of SFR extract in RBL-2H3 cells was 196.85 ${\mu}g$/ml. Both activity of NF-$\kappa$B promoter in RBL-2H3 cells significantly diminished after the dose-dependent treatment of SFR. Therefore, our results indicate that SFR has anti-inflammatory and it may be useful for treating allergic diseases such as atopic dermatitis.

• Journal of Ginseng Research
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• v.41 no.2
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• pp.188-194
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• 2017

Background: Fermented black ginseng (FBG) is processed ginseng by the repeated heat treatment and fermentation of raw ginseng. The protective effect and mechanism of FBG on cisplatin-induced nephrotoxicity was investigated to evaluate its therapeutic potential. Methods: The free radical scavenging activity of FBG was measured using 1,1-diphenyl-2-picrylhydrazyl (DPPH). In addition, the protective effect against cisplatin-induced renal damage was tested in rats. FBG was orally administered every day at a dose of 150 mg/kg body weight for 10 d, and a single dose of cisplatin was administered intraperitoneally (7.5 mg/kg body weight) with 0.9% saline on the $4^{th}$ d. Results: The DPPH radical-scavenging activity of FBG ($IC_{50}=384{\mu}g/mL$) was stronger than that of raw ginseng. The improved DPPH radical-scavenging activity was mediated by the generation phenolic compounds. The decreased cell viability by cisplatin was recovered significantly after treatment with FBG in a dose-dependent manner. Then, the protective effect of FBG on cisplatin-induced oxidative renal damage was investigated in rats. The decreased creatinine clearance levels, which are a reliable marker for renal dysfunction in cisplatin-treated rats, were reduced to the normal level after the administration of FBG. Moreover, FBG showed protective effects against cisplatin-induced oxidative renal damage in rats through the inhibition of $NF-{\kappa}B/p65$, COX-2, and caspase-3 activation. Conclusion: These results collectively show that the therapeutic evidence for FBG ameliorates the nephrotoxicity via regulating oxidative stress, inflammation, and apoptosis.

• Journal of the korean academy of Pediatric Dentistry
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• v.42 no.2
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• pp.180-187
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• 2015

Incontinentia pigmenti, also called Bloch-Sulzberger syndrome, is a rare X-linked inherited dominant disorder that affects females, but causes spontaneous abortion of prenatal males. Incontinentia pigmenti is a systemic disease with clinical features similar to ectodermal dysplasia, including congenitally missing teeth. The pathogenesis is related to gene mutations in NF-kappa-B essential modulator on chromosome Xq28. Incontinentia pigmenti is caused by a defect in the developmental stage of organs originating from the ectoderm or mesoderm and involves the skin, eyes, hair, teeth and central nervous system. This report discusses the management of three cases of 3 to 5 years old females with incontinentia pigmenti and accompanying multiple missing teeth. The cases had sparse hair, and showed oligodontia and anomalous crowns with supplementary cusps in the posterior teeth and conical anterior teeth. Removable space maintainers were applied, achieving improved esthetics, recovery of mastication and increased self-esteem in the patients.

• Biomedical Science Letters
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• v.24 no.3
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• pp.213-220
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• 2018

Triglyceride (TG) is known to be associated with inflammatory disease including atherosclerosis. In a variety of atherosclerosis models, T lymphocytes are localized in the earliest lesions of atherosclerosis. T cell associated cytokines such as $TNF-{\alpha}$ and $IFN-{\gamma}$ have pre-dominant inflammatory effects in chronic vascular diseases. In our previous study, we found that the expression of $TNF-{\alpha}$ and its receptor, $TNF-{\alpha}R$ was increased when Jurkat T lymphocyte cell lines were exposed to TGs. Therefore, experiments were conducted to determine which cell signaling pathway are involved in the increase of $TNF-{\alpha}$ and $TNF-{\alpha}R$ expression by TGs. To identify signal transduction pathways involved in TG-induced upregulation of $TNF-{\alpha}$, we treated TG-exposed Jurkat T cells with specific inhibitors for MEK1, PI3K, $NF-{\kappa}B$ and PKC. We found that inhibition of the MEK1 pathway blocked TG-induced upregulation of $TNF-{\alpha}$. However, the expression level of $TNF-{\alpha}R$ did not change with any signal transduction inhibitor. Based on this observation, we suggest that increase of exogenous TG induces increase of $TNF-{\alpha}$ expression through MEK1 pathway in Jurkat T cells. In addition, it was confirmed that the increase of $TNF-{\alpha}$ and $TNF-{\alpha}R$ expression by TGs occurs via different pathways.