Kim, Jeom-Ji;An, Sang-Il;Lee, Jeon-Su;Yun, Sae-Mi;Lee, Mi-Yeong;Yun, Hyeong-Seon
Korean Journal of Food Science and Technology
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v.40
no.3
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pp.332-336
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2008
Ginger is widely used as a traditional herbal medicine. Both ginger and its extracts have been used to treat many chronic inflammatory conditions via the inhibition of nuclear factor-kappa B (NF-${\kappa}B$) activation, which results in the suppression of cyclooxygenase-2 (COX-2) expression. However, the mechanisms as to how ginger extracts mediate their health effects are largely unknown. Toll-like receptors (TLRs) trigger anti-microbial innate immune responses, recognizing conserved microbial structural molecules that are known as pathogen-associated molecular patterns. All TLR signaling pathways culminate in the activation of NF-${\kappa}B$. The activation of NF- ${\kappa}B$ leads to the induction of inflammatory gene products, including cytokines and COX-2. This study reports the biochemical evidence that 6-shogaol, an active compound in ginger, inhibits NF-${\kappa}B$ activation and COX-2 expression induced by TLR2, TLR3, and TLR4 agonists. Furthermore, 6-shogaol inhibited NF-${\kappa}B$ activation induced by the following downstream signaling components of the TLRs: MyD88, $IKK{\beta}$, and p65. These results imply that ginger can modulate immune responses that could potentially modify the risk of many chronic inflammatory diseases.
BACKGROUND/OBJECTIVES: Several pharmacological properties of red rice extract have been reported including anti-oxidant, anti-tumor, and reduced cancer cell invasion. This study was conducted to evaluate the anti-inflammatory effects of red rice extract on the production of inflammatory mediators in lipopolysaccharide (LPS)-induced Raw 264.7 macrophages. MATERIALS/METHODS: Pro-inflammatory cytokines including tumor necrosis factor-${\alpha}$ and interleukin-6 were determined by ELISA and cyclooxygenase-2 and inducible nitric oxide synthase expression was evaluated using western blot analysis. In addition, the signaling pathway controlling the inflammatory cascade such as nuclear factor kappa B ($NF-{\kappa}B$), activator proteins-1 (AP-1), and mitogen-activated protein kinase (MAPK) was determined. RESULTS: Our results showed that red rice polar extract fraction (RR-P), but not non-polar extract fraction, inhibited interleukin-6, tumor necrosis factor-${\alpha}$, and nitric oxide production in LPS-induced Raw 264.7 cells. RR-P also reduced the expression of inflammatory enzymes, inducible nitric oxide synthase, and cyclooxygenase-2. In addition, activation of AP-1 and $NF-{\kappa}B$ transcription factor in the nucleus was abrogated by RR-P. RR-P inhibited the phosphorylation of extracellular signaling-regulated kinase 1/2, c-Jun NH2-terminal kinase, and p38 MAPK signaling responsible for the expression of inflammatory mediators in LPS-stimulated Raw 264.7 cells. Based on chemical analysis, high amounts of proanthocyanidin and catechins were detected in the RR-P fraction. However, only proanthocyanidin reduced $NF-{\kappa}B$ and AP-1 activation in LPS-activated Raw 264.7 cells. CONCLUSION: These observations suggest that the anti-inflammatory properties of RR-P may stem from the inhibition of pro-inflammatory mediators via suppression of the AP-1, $NF-{\kappa}B$, and MAPKs pathways.
It confirmed the applicability as an anti-inflammatory material from Rubus occidentalis seed (RSE) extract. In HaCaT cells to evaluate the anti-inflammatory potential as a material RSE extract on the activity of the inflammatory factors caused by UVB and $IFN-{\gamma}/TNF-{\alpha}$. We measured the activity of ROS, interleukin-$1{\beta}$ ($IL-1{\beta}$), interleukin-6 (IL-6) and interleukin-8 (IL-8) by ROS-Glo $H_2O_2$ assay and ELISA kit. Our results showed that the RSE extracts inhibit the UVB and $IFN-{\gamma}/TNF-{\alpha}$-induced ROS activities and expression of $IL-1{\beta}$, IL-6 and IL-8 in a dose-dependent manner. Also it was found that inflammatory mediators of the expression of cyclooxygenase-2 (COX-2) inhibition were also brought, the expression of which is increased $PGE_2$ by COX-2 also inhibited. Finally RSE extracts measure the seed expression of filaggrin in the skin barrier, the main factor of the extract could be confirmed to increase the expression of the filaggrin damaged as a result of this concentration-dependent manner. Through this, it was able to confirm that the efficacy RSE extract to protect the inflammation by restoring the damaged layers of the epidermis. Results from more than RSE extract was able to confirm that the extract that has anti-inflammatory effects by improving the inflammation being produced from UVB.
The effects of erlotinib combined with celecoxib in a lung cancer xenograft model were here explored with a focus on possible mechanisms. A xenotransplanted lung cancer model was established in nude mice using the human lung cancer cell A549 cell line and animals demonstrating tumour growth were randomly divided into four groups: control, erlotinib, celecoxib and combined (erotinib and celecoxib). The tumor major axis and short diameter were measured twice a week and after 40 days tissues were collected for immunohistochemical analyses of Bcl-2 and Bax positive cells and Western-blotting analyses for the epidermal growth factor recepto (EGFR), P-EGFR, and cyclooxygenase-2 (COX-2). Tumor size in the combined group was smaller than in the others (p<0.01) and the percentage of Bcl-2 positive cells was fewer in most cases (p<0.01), while that of Bax positive cells was greater than in the erlotinib and celecoxib groups (P>0.05). Western blotting showed decreased expression of P-EGFR and COX-2 with both erlotinib and celecoxib treatments, but most pronouncedly in the combined group (P<0.05). Simultaneous blockage of the EGFR and COX-2 signal pathways exerted stronger growth effects in our human xenotransplanted lung cancer model than inhibition of either pathway alone. The anti-tumor effects were accompanied by synergetic inhibition of tumor cell apoptosis, activation of p-EGFR and expression of COX-2.
In this study, we evaluated the role of apurinic/apyrimidinic endonuclease1/redox factor-1 (Ref-1) on the tumor necrosis factor-$\alpha$ (TNF-$\alpha$) induced cyclooxygenase-2 (COX-2) expression using A549 lung adenocarcinoma cells. TNF-$\alpha$ induced the expression of COX-2 in A549 cells, but did not induce BEAS-2B expression. The expression of COX-2 in A549 cells was TNF-$\alpha$ dose-dependent (5~100 ng/ml). TNF-$\alpha$-stimulated A549 cells evidenced increased Ref-1 expression in a dose-dependent manner. The adenoviral transfection of cells with AdRef-1 inhibited TNF-$\alpha$-induced COX-2 expression relative to that seen in the control cells ($Ad{\beta}gal$). Pretreatment with $10\;{\mu}M$ of SB203580 suppressed TNF-$\alpha$-induced COX-2 expression, thereby suggesting that p38 MAPK might be involved in COX-2 expression in A549 cells. The phosphorylation of p38 MAPK was increased significantly after 5 minutes of treatment with TNF-$\alpha$, reaching a maximum level at 10 min which persisted for up to 60 min. However, p38MAPK phosphorylation was markedly suppressed in the Ref-1-overexpressed A549 cells. Taken together, our results appear to indicate that Ref-1 negatively regulates COX-2 expression in response to cytokine stimulation via the inhibition of p38 MAPK phosphorylation. In the lung cancer cell lines, Ref-1 may be involved as an important negative regulator of inflammatory gene expression.
Objective: To explore the sensitivity of gastric cancer cells to chemotherapy drugs in elderly patients and its correlation with cyclooxygenase-2 (COX-2) expression in cancer tissue. Materials and Methods: Forty-three elderly patients with gastric cancer (observation group) and 31 young patients with gastrointestinal tumors (control group) who were all diagnosed by pathology and underwent surgery in the 89th Hospital of Chinese People's Liberation Army were selected. Drug sensitivity testing of tumor cells in primary culture was carried out in both groups using a methyl thiazolyl tetrazolium (MTT) method, and the expression of COX-2 and the factors related to multi-drug resistance (MDR) in cancer tissue were assessed by immunohistochemistry. Results: The inhibition rates (IR) of vincristine (VCR), 5-fluorouracil (5-FU), oxaliplatin (L-OHP), mitomycin (MMC) and epirubicin (eADM) on tumor cells in the observation group were dramatically lower than in the control group, with statistical significance (P<0.05 or P<0.01). The positive rates of COX-2, glutathione s-transferase-${\pi}$ (GST-${\pi}$) and P glycoprotein (P-gp) expression in cancer tissue in the observation group were all higher than in control group (P<0.05), while that of DNA topoisomerase $II{\alpha}$ ($TopoII{\alpha}$) expression lower than in the control group (P<0.01). In the observation group, COX-2 expression in cancer tissue had a significantly-positive correlation with GST-${\pi}$ and P-gp (r=0.855, P=0.000; r=0.240, P=0.026), but a negative correlation with $TopoII{\alpha}$ (r=-0.328, P=0.002). In the control group, COX-2 expression in cancer tissue was only correlated with P-gp positively (r=0.320, P=0.011). Bivariate correlation analysis displayed that COX-2 expression in cancer tissue in the observation group had a significantly-negative correlation with the IRs of 5-FU, L-OHP, paclitaxel (PTX) and eADM in tumor cells (r=-0.723, P=0.000; r=-0.570, P=0.000; r=-0.919, P=0.000; r=-0.781, P=0.000), but with hydroxycamptothecine (HCPT), VCR and 5-FU in the control group (r=-0.915, P=0.000; r=-0.890, P=0.000; r=-0.949, P=0.000). Conclusions: Gastric cancer cells in elderly patients feature stronger MDR, which may be related to high COX-2 expression.
Kang, Yun-Mi;Jeon, Eun-jin;Chung, Kyung-Sook;Cheon, Se-Yun;Park, Jong Hyuk;Han, Yoo-Chang;An, Hyo-Jin
The Korea Journal of Herbology
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v.32
no.2
/
pp.25-32
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2017
Objectives : This study was conducted to investigate candidate materials as anti-inflammatory agent from extracts of Korean medicinal plants in Hwaak mountain. Ligustrum obtusifolium (LO) is a Korea medicinal plants that commonly used for robustness and hemostasis. It has been reported that LO has exhibited anti-ischemic, anti-oxidative, anti-hypolipidemic, anti-tumor and hypoglycemic effects. However, LO has not been previously reported to have an anti-inflammatory effect. Therefore, we have evaluated the anti-inflammatory effects of LO and its underlying molecular mechanisms in LPS-induced RAW 264.7 macrophages. Methods : Cell viability was determined by MTT assay in RAW 264.7 macrophages. Nitric Oxide (NO) was measured with Griess reagent and pro-inflammatory cytokines were detected by ELISA in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. Protein expressions of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and p65 subunit of nuclear $factor-{\kappa}B$ ($NF-{\kappa}B$) were determined by Western blot analysis. Results : Among 15 extracts of Korean medicinal plants tested, Ligustrum obtusifolium (LO) showed the inhibition of NO production without cytotoxicity. LO reduced the expression levels of iNOS and COX-2 proteins in LPS-simulated RAW 264.7 macrophages in dose-dependent manner. Consistent with these data, LO inhibited the productions of $TNF-{\alpha}$, IL-6, and $IL-1{\beta}$ in LPS-simulated RAW 264.7 macrophages. Furthermore, LO attenuated the LPS-induced nuclear translocation of p65 $NF-{\kappa}B$ in RAW 264.7 macrophages involving suppression of $NF-{\kappa}B$ activation. Conclusions : Taken together, these results suggest that the anti-inflammatory effects of LO is associated with regulation of inflammatory mediators via inhibition of $NF-{\kappa}B$ activation in LPS-treated RAW 264.7 macrophages.
Objective: The purpose of this study is to investigate the combined effects of exemestane and aspirin on MCF-7 human breast cancer cells. Methods: Antiproliferative effects of exemestane and aspirin, alone and in combination, on growth of MCF-7 human breast cancer cells were assessed using the MTT assay. Synergistic interaction between the two drugs was evaluated in vitro using the combination index (CI) method. The cell cycle distribution was analyzed by flow cytometry and Western blotting was used to investigate the expression of cyclooxygenase-1, cyclooxygenase-2 and Bcl-2. Results: MTT assays indicated that combination treatment obviously decreased the viability of MCF-7 human breast cancer cells compared to individual drug treatment (CI<1). In addition, the combination of exemestane and aspirin exhibited a synergistic inhibition of cell proliferation, significantly arrested the cell cycle in the $G_0/G_1$ phase and produced a stronger inhibitory effect on COX-1 and Bcl-2 expression than control or individual drug treatment. Conclusion: These results indicate that the combination of exemestane and aspirin might become a useful method to the treatment of hormone-dependent breast cancer. The combination of the two inhibitors significantly increased the response as compared to single agent treatment, suggesting that combination treatment could become a highly effective approach for breast cancer.
Kristina Lama;Hyehyun Hong;Tae-Jin Park;Jin-Soo Park;Won-Jae Chi;Seung-Young Kim
Journal of Applied Biological Chemistry
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v.66
/
pp.29-38
/
2023
Recent studies have highlighted the link between diseases and inflammation across our lifespan. Our sedentary lifestyle, high-calorie diet, chronic stress, chronic infections, and exposure to pollutants and xenobiotics, collectively intensify the course and recurrence of infections and inflammation in our bodies, promoting the prevalence of chronic diseases and aging. Given such phenomena and considering additional factors such as the frequency of prescription, and easy access to over-the-counter drugs, the need for anti-inflammatory therapeutics is ever-increasing. However, the readily available anti-inflammatory treatment option comes with a greater risk of side effects or high cost (biologics). Therefore in this growing competition of discovering and developing new potent anti-inflammatory drugs, we focused on utilizing the established knowledge of traditional medicine to find lead compounds. Since lead optimization is an indispensable step toward drug development, we applied this concept for the production of potent anti-inflammatory compounds achieved by structural modification of flavonoids. The derivative obtained through acetylation of myricetin, 3,3',4',5,5',7-hexaacetate myricetin, showed a greater inhibitory effect in the production of pro-inflammatory mediators such as nitric oxide, Prostaglandin E2, and pro-inflammatory cytokines like interleukin-6, interleukin1β, in lipopolysaccharide-stimulated RAW264.7 mouse macrophage cells compared to myricetin. The increased potency of inhibition was in conjunction with an increased inhibitory effect on inducible nitric oxide synthase and cyclooxygenase-2 proteins. Through such measures, this study supports lead optimization for well-established lead compounds from traditional medicine using a simpler and greener chemistry approach for the purpose of designing and developing potent anti-inflammatory therapeutics with possibly fewer side effects and increased bioavailability.
Pyeongpaesan (平肺散) has been used in Korea for many centuries as a treatment for respiratory disease. The effect of Pyeongpaesan (平肺散) on tracheal smooth muscle is not known. The purpose of the present study is to determine the effect of Pyeongpaesan (平肺散) on histamine and acetylcholine induced tracheal smooth muscle contraction in rats and guinea pigs. Guinea pig (500 g, male) and Sprague Dawley rats (200 g, male) were killed by $CO_2$ exposure and a segment (8-10 mm) of the thoracic trachea from each rat and guinea pig was cut into equal segments and mounted 'in pairs' in a tissue bath. Contractile force was measured with force displacement transducers under 0.5 g loading tension. The dose of histamine (His) and acetylcholine (Ach) which evoked 50% of maximal response ($ED_{50}$) was obtained from cumulative dose response curves for histamine and acetylcholine $(10^{-7}{\sim}10^{-4}M)$. Contractions evoked by His $(ED_{50})$ and Ach $(ED_{50})$ were inhibited significantly by Pyeongpaesan (平肺散). In guinea pig tracheal smooth muscle, the mean percent inhibition of acetylcholine induced contraction was 13.5% (p<0.05) after $10{\mu}l/ml$ Pyeongpaesan (平肺散), $64.6\(p<0.01)\;after\;30{\mu}l/ml$ Pyeongpaesan (平肺散), and $92.8\(p<0.01)\;after\;100{\mu}l/ml$ Pyeongpaesan (平肺散). In rat tracheal smooth muscle, the mean percent inhibition of acetylcholine induced contraction was $60.9\(p<0.01)\;after\;30{\mu}l/ml$ Pyeongpaesan (平肺散), and $91.2\(p<0.01)\;after\;100{\mu}l/ml$ Pyeongpaesan (平肺散). Also, in guinea pig tracheal smooth muscle, the mean percent inhibition of histamine induced contraction was $104.8\(p<0.01)\;after\;30{\mu}l/ml$ Pyeongpaesan (平肺散) and $142.3\(p<0.01)\;after\;100{\mu}l/ml$ Pyeongpaesan (平肺散). In rat tracheal smooth muscle, the mean percent inhibition of histamine induced contraction was $63.7\(p<0.01)\;after\;30{\mu}l/ml$ Pyeongpaesan (平肺散), and $107.5\(p<0.01)\;after\;100{\mu}l/ml$ Pyeongpaesan (平肺散). Propranolol $(10^{-7}M)$ slightly but significantly attenuated the inhibitory effects of Pyeongpaesan (平肺散). Following treatment with propranolol, the mean percent inhibition caused by $100{\mu}l/ml$ Pyeongpaesan (平肺散) fell to 15.7% (p<0.05) in guinea pig induced by acetylcholine contraction and the mean percent inhibition caused by $100{\mu}l/ml$ Pyeongpaesan (平肺散) fell to 22.3% (p<0.05) in guinea pig induced by histamine contraction and by $100{\mu}l/ml$ Pyeongpaesan (平肺散) fell to 28.7% (p<0.01) in rat induced by histamine contraction. Indomethacin and methylene blue $(10^{-7}\;M)$ did not significantly alter the inhibitory effect of Pyeongpaesan (平肺散). Also, I could find the effects of Pyeongpaesan (平肺散) and Pyeongpaesanga (平肺散加) morphine on the tracheal smooth muscle in guinea pig and rat did not change significantly. These results indicate that Pyeongpaesan. (平肺散) can relax histamine and acetylcholine-induced contraction of guinea pig and rat tracheal smooth muscle, and that this inhibition involves sympathetic effects and the release of cyclooxygenase products.
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