• Title/Summary/Keyword: suppressing activity

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Antifungal Activity-Guided Analysis of Actinostemma lobatum Extracts through Serial Sub-fractions

  • Seonwoo Choi;Song Hee Lee;Byeong Su Hwang;Young Taek Oh;Junhyun Jeon
    • The Plant Pathology Journal
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    • v.40 no.2
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    • pp.218-224
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    • 2024
  • Plants are treasure trove of novel compounds that have potential for antifungal chemicals and drugs. In our previous study, we had screened plant extracts obtained from more than eight hundred plant materials collected in Korea, and found that butanol fraction of the Actinostemma lobatum were most potent in suppressing growth of diverse fungal pathogens of plants. Here in this study, we describe further analysis of the butanol fraction, and summarize the results of subsequent antifungal activity test for the sub-fractions against a selected set of plant pathogenic fungi. This line of analyses allowed us to identify the sub-fractions that could account for a significant proportion of observed antifungal activity of initial butanol fraction from A. lobatum. Further analysis of these sub-fractions and determination of structure would provide the shortlist for novel compounds that can be a lead to new agrochemicals.

Shikonin Isolated from Lithospermum erythrorhizon Downregulates Proinflammatory Mediators in Lipopolysaccharide-Stimulated BV2 Microglial Cells by Suppressing Crosstalk between Reactive Oxygen Species and NF-κB

  • Prasad, Rajapaksha Gedara;Choi, Yung Hyun;Kim, Gi-Young
    • Biomolecules & Therapeutics
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    • v.23 no.2
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    • pp.110-118
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    • 2015
  • According to the expansion of lifespan, neuronal disorder based on inflammation has been social problem. Therefore, we isolated shikonin from Lithospermum erythrorhizon and evaluated anti-inflammatory effects of shikonin in lipopolysaccharide (LSP)-stimulated BV2 microglial cells. Shikonin dose-dependently inhibits the expression of the proinflammatory mediators, nitric oxide (NO), prostaglandin $E_2$ ($PGE_2$), and tumor necrosis factor-${\kappa}B$ (TNF-${\alpha}$) as well as their main regulatory genes and products such as inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), and TNF-${\alpha}$ in LPS-stimulated BV2 microglial cells. Additionally, shikonin suppressed the LPS-induced DNA-binding activity of nuclear factor-${\kappa}B$ (NF-${\kappa}B$) to regulate the key regulatory genes of the proinflammatory mediators, such as iNOS, COX-2, and TNF-${\alpha}$, accompanied with downregulation of reactive oxygen species (ROS) generation. The results indicate that shikonin may downregulate the expression of proinflammatory genes involved in the synthesis of NO, $PGE_2$, and TNF-${\alpha}$ in LPS-treated BV2 microglial cells by suppressing ROS and NF-${\kappa}B$. Taken together, our results revealed that shikonin exerts downregulation of proinflammatory mediators by interference the ROS and NF-${\kappa}B$ signaling pathway.

Screening and Identification of Antimicrobial Compounds from Streptomyces bottropensis Suppressing Rice Bacterial Blight

  • Park, Sait-Byul;Lee, In-Ae;Suh, Joo-Won;Kim, Jeong-Gu;Lee, Choong-Hwan
    • Journal of Microbiology and Biotechnology
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    • v.21 no.12
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    • pp.1236-1242
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    • 2011
  • Xanthomonas oryzae pv. oryzae (Xoo) is the most devastating pathogen to Oryza sativa and has been shown to cause bacterial blight. Two bioactive compounds showing antimicrobial activities against Xoo strain KACC 10331 were isolated from a Streptomyces bottropensis strain. The ethyl acetate extract was fractionated on a Sephadex LH-20 column, and then purified by preparative HPLC. The purified compounds were identified as bottromycin A2 and dunaimycin D3S by HR/MS and $^1H$ NMR analyses. The MIC value against Xoo and the lowest concentration still capable of suppressing rice bacterial blight were 2 ${\mu}g$/ml and 16 ${\mu}g$/ml for bottromycin A2, and 64 ${\mu}g$/ml and 0.06 ${\mu}g$/ml for dunaimycin D3S, respectively. These two compounds were shown to exert different bioactivities in vitro and in rice leaf explants.

Suppressing breast cancer by exercise: consideration to animal models and exercise protocols

  • Lee, Jea Jun;Beak, Suji;Ahn, Sang Hyun;Moon, Byung Seok;Kim, Jisu;Lee, Kang Pa
    • Korean Journal of Exercise Nutrition
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    • v.24 no.2
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    • pp.22-29
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    • 2020
  • [Purpose] Exercise is thought to have a significant effect on chemotherapy, and previous studies have reported that exercise can increase patient survival. Thus, in this review, we aimed to summarize various animal models to analyze the effects of exercise on breast cancer. [Methods] We summarized types of breast cancer animal models from various reports and analyzed the effects of exercise on anti-cancer factors in breast cancer animal models. [Results] This review aimed to systematically investigate if exercise could aid in suppressing breast cancer. Our study includes (a) increase in survival rate through exercise; (b) the intensity of exercise should be consistent and increased; (c) a mechanism for inhibiting carcinogenesis through exercise; (d) effects of exercise on anti-cancer function. [Conclusion] This review suggested the necessity of a variety of animal models for preclinical studies prior to breast cancer clinical trials. It also provides evidence to support the view that exercise plays an important role in the prevention or treatment of breast cancer by influencing anticancer factors.

Celastrol ameliorates cytokine toxicity and pro-inflammatory immune responses by suppressing NF-κB activation in RINm5F beta cells

  • Ju, Sung Mi;Youn, Gi Soo;Cho, Yoon Shin;Choi, Soo Young;Park, Jinseu
    • BMB Reports
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    • v.48 no.3
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    • pp.172-177
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    • 2015
  • Upregulation of pro-inflammatory mediators contributes to ${\beta}$-cell destruction and enhanced infiltration of immune cells into pancreatic islets during development of type 1 diabetes mellitus. In this study, we examined the regulatory effects and the mechanisms of action of celastrol against cytotoxicity and pro-inflammatory immune responses in the RINm5F rat pancreatic ${\beta}$-cell line stimulated with a combination of interleukin-1 beta, tumor necrosis factor-alpha, and interferon-${\gamma}$. Celastrol significantly restored cytokine-induced cell death and significantly inhibited cytokine-induced nitric oxide production. In addition, the protective effect of celastrol was correlated with a reduction in pro-inflammatory mediators, such as inducible nitric oxide synthase, cyclooxygenase-2, and CC chemokine ligand 2. Furthermore, celastrol significantly suppressed cytokine-induced signaling cascades leading to nuclear factor kappa B (NF-${\kappa}B$) activation, including $I{\kappa}B$-kinase (IKK) activation, $I{\kappa}B$ degradation, p65 phosphorylation, and p65 DNA binding activity. These results suggest that celastrol may exert its cytoprotective activity by suppressing cytokine-induced expression of pro-inflammatory mediators by inhibiting activation of NF-${\kappa}B$ in RINm5F cells.

Gomisin G Inhibits the Growth of Triple-Negative Breast Cancer Cells by Suppressing AKT Phosphorylation and Decreasing Cyclin D1

  • Maharjan, Sony;Park, Byoung Kwon;Lee, Su In;Lim, Yoonho;Lee, Keunwook;Kwon, Hyung-Joo
    • Biomolecules & Therapeutics
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    • v.26 no.3
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    • pp.322-327
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    • 2018
  • A type of breast cancer with a defect in three molecular markers such as the estrogen receptor, progesterone receptor, and human epidermal growth factor receptor is called triple-negative breast cancer (TNBC). Many patients with TNBC have a lower survival rate than patients with other types due to a poor prognosis. In this study, we confirmed the anti-cancer effect of a natural compound, Gomisin G, in TNBC cancer cells. Treatment with Gomisin G suppressed the viability of two TNBC cell lines, MDA-MB-231 and MDA-MB-468 but not non-TNBC cell lines such as MCF-7, T47D, and ZR75-1. To investigate the molecular mechanism of this activity, we examined the signal transduction pathways after treatment with Gomisin G in MDA-MB-231 cells. Gomisin G did not induce apoptosis but drastically inhibited AKT phosphorylation and reduced the amount of retinoblastoma tumor suppressor protein (Rb) and phosphorylated Rb. Gomisin G induced in a proteasome-dependent manner a decrease in Cyclin D1. Consequently, Gomisin G causes cell cycle arrest in the G1 phase. In contrast, there was no significant change in T47D cells except for a mild decrease in AKT phosphorylation. These results show that Gomisin G has an anti-cancer activity by suppressing proliferation rather than inducing apoptosis in TNBC cells. Our study suggests that Gomisin G could be used as a therapeutic agent in the treatment of TNBC patients.

Luteolin Induces Apoptosis via Mitochondrial Pathway and Inhibits Invasion and Migration of Oral Squamous Cell Carcinoma by Suppressing Epithelial-Mesenchymal Transition Induced Transcription Factors

  • Park, Bong-Soo;Kil, Jong-Jin;Kang, Hae-Mi;Yu, Su-Bin;Park, Dan-Bi;Park, Jin-A;Kim, In-Ryoung
    • International Journal of Oral Biology
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    • v.43 no.2
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    • pp.69-76
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    • 2018
  • Oral squamous cell carcinoma (OSCC) is the most common type of oral malignancy. Numerous therapies have been proposed for its cure. Research is continually being conducted to develop new forms of treatment as current therapies are associated with numerous side-effects. Luteolin, a common dietary flavonoid, has been demonstrated to possess strong anti-cancer activity against various human cancer cell lines. Nevertheless, research into luteolin-based anticancer activity against oral cancer remains scarce. Thus, the objective of this study was to assess the effect of luteolin as an anti-cancer agent. After treatment with luteolin, Ca9-22 and CAL-27 oral cancer cells showed condensed nuclei and enhanced apoptotic rate with evidence of mitochondria-mediated apoptosis. Epithelialmesenchymal transition (EMT) is closely related to tumor migration and invasion. Luteolin suppressed cancer cell invasion and migration in the current study. Elevated expression of E-cadherin, an adherens junction protein, was evident in both cell lines after luteolin treatment. Luteolin also significantly inhibited transcription factors (i.e., N-cadherin, Slug, Snail, Twist, and ZEB-1) that regulated expression of tumor suppressors such as E-cadherin based on Western blot analysis and quantitative PCR. Thus, luteolin could induce mitochondrial apoptosis and inhibit cancer cell invasion and migration by suppressing EMT-induced transcription factors.

Effects of Corydalis Tuber on Synthesis of NO and $PGE_2$ in Murine Macrophage RAW 264.7 Cells Stimulated by LPS

  • Lee, Ki-Young;Park, Se-Keun;Kim, Jeong-Seon;Jang, Mi-Hyeon;Kim, Chang-Ju;Choi, Sun-Mi;Lee, Hye-Jung;Kim, Ee-Hwa
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.19 no.3
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    • pp.785-791
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    • 2005
  • Corydalis Tuber has traditionally been used for the treatment of water retention in the body. Administration of the aqueous extract of Corydalis Tuber has been known to be effective for the control of pain and treatment of arthritis. It was reported that Corydalis Tuber possesses anti-inflammatory activity and modulates the intestinal immune system. The effect of Corydalis Tuber against LPS-stimulated expressions of COX-2, iNOS, and $IL-1{\beta}$ in cells of the murine RAW 264.7 macrophages was investigated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, reverse transcription-polymerase chain reaction (RT-PCR), $PGE_2$ immunoassay, and NO detection. The aqueous extract of Corydalis Tuber was shown to suppress $PGE_2$ production by inhibition on the LPS-stimulated enhancement of COX-2 enzyme activity, $IL-1{\beta}$, and iNOS expression in the RAW 264.7 macrophages. Present results suggest that Corydalis Tuber exerts anti-inflammatory and analgesic effects probably by suppressing of COX-2, iNOS, and $IL-1{\beta}$ expressions, resulting in inhibition of $PGE_2$ synthesis. Corydalis Tuber has anti-inflammatory and analgesic effects probably by suppressing of COX-2, iNOS, and $IL-1{\beta}$ mRNA expressions, resulting in inhibition of $PGE_2$ and NO synthesis.

Growth-Suppressing Activity of the Transfected Cx26 on BICR-M1Rk Breast Cancer Cell Line

  • Lee, Hae-Jung;Rhee, Seung-Keun
    • Journal of Microbiology and Biotechnology
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    • v.21 no.5
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    • pp.477-482
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    • 2011
  • There are accumulating evidences suggesting that connexin (Cx), a gap junction channel-forming protein, acts as a growth suppressor in various cancer cells, and this effect is attributeed to the gap junction-mediated intercellular communication (GJIC). In order to characterize the relationship between the growth-arresting activity of Cx26 and its cytoplasmic localizations after expression, we linked a nuclear export signal (NES) sequence to Cx26 cDNA before transfecting into a rat breast cancer cell line. A confocal fluorescent microscopic observation revealed that the insertion of NES minimized the nuclear expression of Cx26, and increased its cytoplasmic expression, including plasma membrane junctions. Total cell counting and BrdUrd-labeling experiments showed that the growth of the breast cancer cells was inhibited by 74% upon transfection of Cx26-NES, whereas only 9% inhibition was observed with only Cx26 cDNA.

3,4-Dihydroxytoluene suppresses UVB-induced wrinkle formation by inhibiting Raf-1

  • Park, Sang-Hee;Kang, Nam Joo
    • Korean Journal of Food Science and Technology
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    • v.52 no.4
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    • pp.385-395
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    • 2020
  • This study examined the effect of 3,4-dihydroxytoluene (DHT) on UVB-induced photoaging and determined its molecular mechanisms, using HaCaT human keratinocytes and SKH-1 hairless mice. DHT suppressed UVB-induced matrix metalloproteinase-1 (MMP-1) expression in HaCaT cells. In vivo data from mouse skin supported that DHT decreased UVB-induced wrinkle formation, epidermal thickness, and matrix metalloproteinase-13 (MMP-13) expression. DHT appeared to exert its anti-aging effects by suppressing UVB-induced Raf-1 kinase activity and subsequent attenuation of UVB-induced phosphorylation of MEK, ERK, and p90RSK in HaCaT cells. In vitro and in vivo pull-down assays revealed that DHT bound with Raf-1 in ATP-noncompetitive manner. Overall, DHT appears to anti-photoaging effects in vitro and in vivo through the suppression of Raf-1 kinase activity and may have potential as a treatment for the prevention of skin aging.