• Journal of Ginseng Research
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• v.43 no.3
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• pp.335-341
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• 2019

Background: Inflammation is a host-defensive innate immune response to protect the body from pathogenic agents and danger signals induced by cellular changes. Although inflammation is a host-defense mechanism, chronic inflammation is considered a major risk factor for the development of a variety of inflammatory autoimmune diseases, such as rheumatic diseases. Rheumatic diseases are systemic inflammatory and degenerative diseases that primarily affect connective tissues and are characterized by severe chronic inflammation and degeneration of connective tissues. Ginseng and its bioactive ingredients, genocides, have been demonstrated to have antiinflammatory activity and pharmacological effects on various rheumatic diseases by inhibiting the expression and production of inflammatory mediators. Methods: Literature in this review was searched in a PubMed site of National Center for Biotechnology Information. Results: The studies reporting the preventive and therapeutic effects of ginseng and ginsenosides on the pathogenesis of rheumatic diseases were discussed and summarized. Conclusion: Ginseng and ginsenosides play an ameliorative role on rheumatic diseases, and this review provides new insights into ginseng and ginsenosides as promising agents to prevent and treat rheumatic diseases.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2020.08a
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• pp.87-87
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• 2020

In this study, we investigated the immune-enhancing activity of water extracts from Hydrangea macrophylla subsp. serrata (WE-HML). WE-HML increased cell viability and production of immunomodulators, which contributed to activating phagocytic activity in RAW264.7 cells. Inhibition of JNK and NF-κB reduced the production of immunomodulators by WE-HML. ROS inhibition suppressed the production of immunomodulators, and the activation of JNK and NF-κB signaling by WE-HML. TLR4 inhibition attenuated the production of immunomodulators, and activation of JNK and NF-κB signaling by WE-HML. In the immunosuppressed mouse model, WE-HML increased the spleen index, the levels of the cytokines, the numbers of white blood cells, lymphocytes, and neutrophils. However, WE-HML inhibited LPS-mediated overproduction of pro-inflammatory mediators in RAW264.7 cells, which indicated that WE-HML may have anti-inflammatory activity under excessive inflammatory conditions. Taken together, WE-HML may be considered to have immune-enhancing activity and expected to be used as a potential immune-enhancing agent.

• Korean Journal of Microbiology
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• v.52 no.4
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• pp.421-427
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• 2016

Acne is known as the most common skin disease. It commonly occurs during adolescents, but it is also present in children and adults because of air pollution, drug abuse and so on. In addition to the hormonal, genetic and environmental factors, Propionibacterium acnes (P. acnes) have also critical roles in outbreak of acne by inducing inflammatory mediators. Increase of sebum production provides an ideal environment for P. acnes that induce inflammation on the skin by activation of monocytic cells and stimulation of inflammatory cytokines. In this study, natural extracts were investigated for anti-inflammatory effects against inflammatory acne by P. acnes infection in terms of reducing cytokine production. Eucalyptus globulus extracts effectively suppressed mRNA synthesis of inflammatory mediators such as $TNF-{\alpha}$, $IL-1{\beta}$, IL-2, and NLRP3 in P. acnes-activated macrophages. Moreover, Eucalyptus globulus extracts inhibit activation of transcription factors, $NF-{\kappa}B$ and NFAT, which are known as key regulators of inflammatory cytokine production. This study suggests the potential of using Eucalyptus globulus extracts as alternative agents for the treatment of acne.

• Korean Journal of Medicinal Crop Science
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• v.24 no.3
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• pp.228-236
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• 2016

Background: Sedum takesimense Nakai has been used as folk medicine in Korea. The present study aimed to determine the biological activity of S. takesimense by investigating the anti-inflammatory effects of S. takesimense water extract (SKLC) on the lipopolysaccharide-induced inflammatory response in RAW 264.7 cells. Methods and Results: Cytotoxicity of SKLC on RAW 264.7 cells was determinded by performing MTS assay was found to have no cytotoxic effect on RAW 264.7 cells at a concentration range of $62-500{\mu}g/m{\ell}$. Further, pretreatment of SKLC inhibited lipopolysaccharide-induced nitric oxide (NO) production in a dose-dependent manner. To determined the inhibitory mechanisms of SKLC on inflammatory mediators, we assessed the inducible nitric oxide synthase (iNOS) and cyclooxygnease-2 (COX-2) pathways. The activities of these pathways were decreased in a dose-dependent manner by SKLC. The production of tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), interleukin $(IL)-1{\beta}$, and IL-6 were also reduced. Conclusions: These results suggest that the down regulation of iNOS, COX-2, TNF-${\alpha}$, IL-$1{\beta}$, and IL-6 expression by SKLC are mediated by the down regulation of nuclear factor-${\kappa}B$ (NF-${\kappa}B$) activity, a transcription factor necessary for pro-inflammatory mediators. This might be the mechanism underlying the anti-inflammatory effects of SKLC.

• The Journal of Korean Medicine
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• v.43 no.1
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• pp.18-32
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• 2022

Objectives: This study aimed to examine the safety, effects on proliferation of hair papilla cells, and anti-inflammatory and antioxidant mechanisms of Artemisia sieversiana Ehrh. ex Willd. (AS) extract. Methods: Safety tests through purity testing, acute toxicity tests, and repeated toxicity tests were performed using AS extract (ASE) which had been dried for over two years. Cell culture and proliferation tests were conducted; VEGF (vascular endothelial growth factor), bFGF (basic fibroblast growth factor), and EGF (epidermal growth factor) and protein expression analyses were performed for mechanistic evaluation; and inhibitory effects of ASE on the RNA expression of testosterone, 5𝛼-reductase, and aromatase was assessed. The anti-inflammatory and antioxidant efficacy of ASE was confirmed by measuring the levels of nitric oxide, inflammatory mediators (TNF-𝛼 and PGE2), inflammatory cytokines (IL-1𝛽, IL-6, and IL-8), and chemokine MCP-1. Results: The safety of ASE was confirmed. The mechanism of cell proliferation in human hair follicle dermal papilla cells involved the promotion of VEGF, bFGF, and EGF expression. ASE decreased mRNA expression of testosterone, 5𝛼-reductase, and aromatase-1 in a concentration-dependent manner. PGE2 and TNF-𝛼 production by inflammatory mediators was also significantly decreased in a concentration-dependent manner, and inflammatory cytokine and chemokine expression was inhibited. Conclusions: ASE is suggested to promote papillary cell growth at the cellular level, to suppress expression of various enzymes involved in hair cycle and cell death, and to inhibit hair loss through anti-androgen, anti-inflammatory, and antioxidant effects.

• Biomolecules & Therapeutics
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• v.31 no.5
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• pp.536-543
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• 2023

Phytoceramide (Pcer) is found mainly in plants and yeast. It can be neuroprotective and immunostimulatory on various cell types. In this study, the therapeutic effect of Pcer was explored using the carrageenan/kaolin (C/K)-induced arthritis rat model and fibroblast-like synoviocytes (FLS). Pcer treatment (1, 10, and 30 mg/kg/day) were given to the arthritic rats for 6 days after disease induction. Weight distribution ration (WDR), knee thickness, squeaking score, serum levels of proinflammatory mediators, and histological analysis were measured and performed to evaluate arthritic symptoms in the rat model. In interleukin (IL)-1β-stimulated FLS, proinflammatory mediators were measured after Pcer (1-30 µM) treatment. Arthritic symptoms in rats with Pcer treatment were significantly decreased at days 4 to 6 after C/K arthritis induction. Inflammation in the knee joints were also significantly decreased in rats with Pcer treatment. Furthermore, in IL-1β-stimulated FLS, the expressions of proinflammatory mediators were also inhibited by Pcer. As shown by the results, Pcer has anti-arthritic effects in the C/K rat model and in synovial cells, suggesting that Pcer has the potential to be a useful agent in arthritis treatment.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2023.04a
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• pp.47-47
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• 2023

Paeonia lactiflora roots (PLR) are a medicinal plant widely used for treating inflammatory diseases. However, PLR has been recently reported to increase the production of proinflammatory mediators and activates phagocytosis in macrophages. Thus, in this study, we tried to verify the macrophage activation of PLR and elucidate its mechanism of action. PLR upregulated the production of proinflammatory mediators and activated phagocytosis in RAW264.7 cells. However, these effects were reversed by inhibition of TLR2/4. In addition, the inhibition of p38, JNK, and ERK1/2 reduced the PLR-mediated production of proinflammatory mediators, and the PLR-mediated activation of p38, JNK, and ERK1/2 was blocked by the TLR4 inhibition. These findings indicate that PLR may activate macrophages through TLR4-dependent activation of p38, JNK, and ERK1/2. These indicate that PLR has immunostimulatory activity. Thus, it is believed that PLR can be used as a functional food agent that enhances the immune system.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2022.09a
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• pp.89-89
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• 2022

Paeonia lactiflora (P. lactiflora) is a medicinal plant widely used for treating inflammatory diseases. However, P. lactiflora has been recently reported to increase the production of proinflammatory mediators and activates phagocytosis in macrophages. Thus, in this study, we tried to verify the macrophage activation of Paeoniae Radix Alba (PRR, also known as red peony root) and elucidate its mechanism of action. PRR upregulated the production of proinflammatory mediators and activated phagocytosis in RAW264.7 cells. However, these effects were reversed by inhibition of TLR2/4. In addition, the inhibition of p38, JNK, and ERK1/2 reduced the PRR-mediated production of proinflammatory mediators, and the SPL-mediated activation of p38, JNK, and ERK1/2 was blocked by the TLR4 inhibition. These findings indicate that PRR may activate macrophages through TLR4-dependent activation of p38, JNK, and ERK1/2. These indicate that PRR has immunostimulatory activity. Thus, it is believed that PRR can be used as a functional food agent that enhances the immune system.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.8
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• pp.4553-4557
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• 2013

Objective: The purpose of this study was to identify genes related to bladder cancer with samples from normal and disease cases by microarray chip. Methods: After downloading the gene expression profile GSE3167 from Gene Expression Omnibus database which includes 50 bladder samples, comprising 9 normal and 41 disease samples, differentially expressed genes were identified with packages in R language. The selected differentially expressed genes were further analyzed using bioinformatics methods. Firstly, molecular functions, biological processes and cell component analysis were researched by software Gestalt. Then, software String was used to search interaction relationships among differentially expressed genes, and hub genes of the network were selected. Finally, by using plugins of software Cytoscape, Mcode and Bingo, module analysis of hub-genes was performed. Results: A total of 221 genes were identified as differentially expressed by comparing normal and disease bladder samples, and a network as well as the hub gene C1QBP was obtained from the network. The C1QBP module had the closest relationship to production of molecular mediators involved in inflammatory responses. Conclusion: We obtained differentially expressed genes of bladder cancer by microarray, and both PRDX2 and YWHAZ in the module with hub gene C1QBP were most significantly related to production of molecular mediators involved in inflammatory responses. From knowledge of inflammatory responses and cancer, our results showed that, the hub gene and its module could induce inflammation in bladder cancer. These related genes are candidate bio-markers for bladder cancer diagnosis and might be helpful in designing novel therapies.

• The Korea Journal of Herbology
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• v.30 no.1
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• pp.85-93
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• 2015

Objectives : Bilobalide (BIL) is a predominant sesquiterpene trilactone constituent that accounts for a partial portion of the standardized Ginkgonis Folium extract, which has been widely used to treat a variety of neurological disorders involving cerebral ischemia and neurodegeneration. In this study, it was tested whether BIL exhibits anti-inflammatory activities on inflammation response, or not. Methods : To elucidate the molecular mechanisms of BIL on pharmacological and biochemical actions in inflammation, we examined the effect of BIL on pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated macrophages. The investigation was focused on how BIL affect on inflammation-related mediators including various signals such as nitric oxide (NO), prostaglandin $E_2$ ($PGE_2$), inducible NO synthase(iNOS), cyclooxygenase-2(COX-2), interleukin-6(IL-6), tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$), mitogen-activated protein kinases(MAPKs) and nuclear factor kappa-light-chain-enhancer of activated B cells ($NF-{\kappa}B$) in LPS-stimulated RAW 264.7 cells. Results : We found that BIL inhibited LPS-induced NO, $PGE_2$, IL-6 and $TNF-{\alpha}$ productions as well as the expressions of iNOS and COX-2. Furthermore, BIL suppressed the LPS-induced phosphorylation for MAPK activation. Conclusions : These results suggest that BIL has inhibitory effects on LPS-induced $PGE_2$, NO, IL-6 and $TNF-{\alpha}$ production, as well as the expressions of iNOS and COX-2 in the murine macrophage. It seems that these inhibitory effects occur by blocking the phosphorylation of MAPKs for activation. Then, BIL suppressed the activation of nuclear factor $NF-{\kappa}B$ in nucleus. These observations suggest that BIL has anti-inflammatory effect by inhibiting.