• Membrane and Water Treatment
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• v.2 no.1
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• pp.63-74
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• 2011

A spiral wound nanofiltration (NF) membrane (GE Osmonics, DK 4040F) was used to remove pesticides from water. Several solutions of single pesticides and their mixtures were prepared. The pesticides initial concentration ranged from ca. 50 ng/L (single pesticide) to ca. 700 ng/L (as sum of 14 pesticides) and progressively increased with time since the NF experiments were carried out in a concentration mode up to a Volume Concentration Ratio, VCR = 10. Permeate flux and pesticides retention were evaluated as a function of the Volume Concentration Ratio. The permeate flux did not practically change by varying VCR. Pesticide retention was found to be around 97-98% both in the cases of single pesticide solutions and different mixtures of pollutants, and was not affected by the VCR. Pesticides concentration in permeate samples was found to be lower than the maximum concentration level fixed in European directive.

• Journal of Life Science
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• v.21 no.10
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• pp.1415-1421
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• 2011

The purpose of this study was to identify the effects of an L-arginine supplementation and regular exercise training on NF-${\kappa}B$, TNF-${\alpha}$, iNOS, Cav-1, eNOS and Ang II in the aortas of D-galactose (D-gal) induced aging rats. The male Strague-Dawley rats were treated with a D-galactose aging inducing agent; the D-gal injection (50 mg/kg) was given intraperitoneally for 12 wk. Experimental groups were divided into five groups: (1) Young control group (Y-Con, n=8), (2) Aging control group (A-Con, n=8), (3) Aging exercise group (A-Ex, n=8), (4) Aging exercise group with L-arginine supplementation group (A-Ex+A, n=8), and (5) Aging with L-arginine supplementation group (A-A, n=8). The exercise consisted of running on a treadmill for 60 min/day at 20 m/min for 6 day/wk, at 0% gradient for 12 wk. The L-arginine supplementation was given orally at a dose of 150 mg/kg/day for 12 wk. The findings of this study were as follows: 1. NF-${\kappa}B$, TNF-${\alpha}$, iNOS, Cav-1 and Ang II proteins in the aortas of D-gal induced rats were significantly increased, however, L-arginine supplementation and regular exercise resulted in a significant inhibition in the expression of NF-${\kappa}B$, TNF-${\alpha}$, iNOS, Cav-1 and Ang II proteins. 2. eNOS protein in the aortas of D-gal induced rats was significantly decreased, however, L-arginine supplementation and regular exercise resulted in a significant increase in the expression of eNOS proteins. In conclusion, the findings of the present study reveal that L-arginine supplementation alone or regular exercise alone or in combination with L-arginine supplementation for 12 wk increases anti-inflammatory effects by decreasing NF-${\kappa}B$, TNF-${\alpha}$, and iNOS protein expressions within the aortic tissue. In addition, L-arginine supplementation alone or regular exercise alone or in combination with L-arginine supplementation may prevent endothelial function by up-regulation of eNOS protein in the aortas of D-gal induced aging rats.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.2
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• pp.127-134
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• 2018

Myofibrillogenesis regulator-1 (MR-1) is a novel protein involved in cellular proliferation, migration, inflammatory reaction and signal transduction. However, little information is available on the relationship between MR-1 expression and the progression of atherosclerosis. Here we report atheroprotective effects of silencing MR-1 in a model of Ang II-accelerated atherosclerosis, characterized by suppression focal adhesion kinase (FAK) and nuclear factor kappaB ($NF-{\kappa}B$) signaling pathway, and atherosclerotic lesion macrophage content. In this model, administration of the siRNA-MR-1 substantially attenuated Ang II-accelerated atherosclerosis with stabilization of atherosclerotic plaques and inhibited FAK, Akt, mammalian target of rapamycin (mTOR) and NF-kB activation, which was associated with suppression of inflammatory factor and atherogenic gene expression in the artery. In vitro studies demonstrated similar changes in Ang II-treated vascular smooth muscle cells (VSMCs) and macrophages: siRNA-MR-1 inhibited the expression levels of proinflammatory factor. These studies uncover crucial proinflammatory mechanisms of Ang II and highlight actions of silencing MR-1 to inhibit Ang II signaling, which is atheroprotective.

• Molecules and Cells
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• v.45 no.7
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• pp.465-478
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• 2022

MicroRNAs (miRNAs) are a class of small non-coding RNAs that regulate the expression of target messenger RNA (mRNA) complementary to the 3' untranslated region (UTR) at the post-transcriptional level. Hsa-miR-422a, which is commonly known as miRNA derived from transposable element (MDTE), was derived from short interspersed nuclear element (SINE). Through expression analysis, hsa-miR-422a was found to be highly expressed in both the small intestine and liver of crab-eating monkey. AT-Rich Interaction Domain 5 B (ARID5B) was selected as the target gene of hsa-miR-422a, which has two binding sites in both the exon and 3'UTR of ARID5B. To identify the interaction between hsa-miR-422a and ARID5B, a dual luciferase assay was conducted in HepG2 cell line. The luciferase activity of cells treated with the hsa-miR-422a mimic was upregulated and inversely downregulated when both the hsa-miR-422a mimic and inhibitor were administered. Nuclear factor erythroid-2 (NF-E2) was selected as the core transcription factor (TF) via feed forward loop analysis. The luciferase expression was downregulated when both the hsa-miR-422a mimic and siRNA of NF-E2 were treated, compared to the treatment of the hsa-miR-422a mimic alone. The present study suggests that hsa-miR-422a derived from SINE could bind to the exon region as well as the 3'UTR of ARID5B. Additionally, hsa-miR-422a was found to share binding sites in ARID5B with several TFs, including NF-E2. The hsa-miR-422a might thus interact with TF to regulate the expression of ARID5B, as demonstrated experimentally. Altogether, hsa-miR-422a acts as a super enhancer miRNA of ARID5B by collaborating with TF and NF-E2.

• Journal of The Korean Society of Integrative Medicine
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• v.8 no.4
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• pp.163-169
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• 2020

Purpose : This study aimed to investigate the anti-allergic effect of Persicaria perfoliata water extract (PPWE) on IgE stimulated rat basophilic leukemia (RBL-2H3) cell line. Methods : P. perfoliata (L.) H. Gross has been used in traditional medicine as an anti-allergic agent, antipyretic, and diuretic and for respiratory disorders. To analyze the anti-allergic activity of PPWE, release of β-hexosaminidase in RBL-2H3 cells was estimated by enzyme linked immunosorbant assay (ELISA). Also, the cytotoxic effect of PPWE was identified by WST assay, and nuclear factor (NF)-κB and its upstream signaling molecules were assessed by western blot analysis. Results : PPWE treatment significantly attenuated β-hexosaminidase release in a dose dependent manner without any cytotoxicity. PPWE inhibited β-hexosaminidase activity by 38.4±1.2, 36.6±0.6, 32.5±2.2 and 26.5±1.2 at 500, 250, 100, and 50 ㎍/㎖ of PPWE, respectively, compared with the control group. In addition, an analysis of the expression level of NF-κB, an inflammation transcription factor, in RBL-2H3 cells upon IgE stimulation provided reults consistent with the results of β-hexosaminidase release. The phosphorylated status of upstream signaling molecules for transcription factor, mitogen activated protein kinases (MAPKs), was also analyzed. The results showed that PPWE treatment dose-dependently inhibited phosphorylation of extracellular regulatory kinase (ERK) and c-Jun N-terminal kinase (JNK). These results show that PPWE had a strong IgE-mediated degranulation inhibitory effect on RBL-2H3 cells. Conclusion : P. perfoliata ameliorated IgE-mediated allergic reaction via the modulation of MAPK and NF-κB signaling pathway in RBL-2H3 cells. These results indicate that P. perfoliata could be a potential candidate for a treatment strategy against various allergic disorders.

• Korean Journal of Plant Resources
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• v.34 no.3
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• pp.203-215
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• 2021

Bok choy is one of Brassica vegetables widely consumed worldwide. Brassica vegetables have been reported to exert various pharmacological activities such as antioxidant, anti-cancer and cardioprotective activity. However, studies on immunostimulatory activity of bok choy sprout have not been conducted properly. Thus, in this study, we investigated in vitro immunostimulatory activity of bok choy sprout extract (BCS) using mouse macrophage RAW264.7 cells. Our results showed that BCS increased the production of immunomodulators such as NO, iNOS, IL-1β, IL-6, IL-12, TNF-α and MCP-1, and phagocytic activity in RAW264.7 cells. BCS activated MAPK, NF-κB and PI3K/AKT signaling pathways. However, BCS-mediated production of immunomodulators was dependent on JNK, NF-κB and PI3K/AKT signaling pathways. the mRNA expression of TLR2 were significantly increased by BCS, TLR2 inhibition by anti-TLR2 dramatically suppressed the production of immunomodulators by BCS. In addition, TLR2 inhibition by anti-TLR2 significantly reduced BCS-mediated phosphorylation level of AKT, JNK and NF-κB. From these results, BCS may have immunostimulatory activity via TLR2-MAPK, NF-κB and PI3K/AKT signaling pathways. Therefore, BCS expected to be used as a potential immune-enhancing agent.

• Journal of Applied Biological Chemistry
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• v.57 no.2
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• pp.113-122
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• 2014

A5E is complex of several medicinal herb ethanol extracts. The aim of this study is investigating the anticancer effect for non-small cell lung cancer. The antitumor effects of A5E on NCI-H460 were examined by regulation of cell proliferation, apoptosis, cell cycle arrest, mitochondrial membrane potential (${\Delta}{\Psi}_m$), and apoptosis-related protein. Cell proliferation was measured by MTS assay. Apoptosis induced by A5E was confirmed by Annexin V-fluorescein isothiocyanate (FITC)/Propidium Iodide (PI) staining, and cell cycle arrest was measured by PI staining. NF-${\kappa}B$ translocation was detected by immunofluorescence and MMP (${\Delta}{\Psi}_m$) was measured by JC-1 staining. The expression of extrinsic pathway molecules such as FasL and FADD were elevated, and procaspase-8 was processed by A5E. In addition, intrinsic pathway related molecules were altered. The Bcl-2 and Bcl-xl levels decreased, Bax increased, and cytochrome C was released. In addition, the mitochondrial membrane potential collapsed, and caspase-3 and poly-(ADP-ribose) polymerase were processed by A5E. Moreover, A5E affected the cellular survival pathway involving phosphatidylinositol 3-kinase (PI3K)/Akt and NF-${\kappa}B$. PI3K and Akt were downregulated, also NF-${\kappa}B$ expression was decreased, and nuclear translocalization was inhibited by A5E. These results suggested that A5E delays proliferation, inhibit cell cycle progression and induce apoptosis in human lung cancer cell. We conclude that A5E is a potential anticancer agent for human lung carcinoma.

• Journal of Embryo Transfer
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• v.32 no.3
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• pp.209-220
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• 2017

The estrogen-mediated effect of mesenchymal stem cells (MSCs) is a highly critical factor for the clinical application of MSCs. However, the present study is conducted on MSCs derived from adult donors, which have different physiological status with steroid hormonal changes. Therefore, we explores the important role of $17{\beta}$-estradiol (E2) in MSCs derived from female and male newborn piglets (NF- and NM-pBMSCs), which are non-sexually matured donors with steroid hormones. The results revealed that in vitro treatment of MSCs with E2 improved cell proliferation, but the rates varied according to the gender of the newborn donors. Following in vitro treatment of newborn MSCs with E2, mRNA levels of Oct3/4 and Sox2 increased in both genders of MSCs and they may be correlated with both estrogen receptor ${\alpha}$ ($ER{\alpha}$) and $ER{\beta}$ in NF-pBMSCs, but NM-pBMSCs were only correlated with $ER{\alpha}$. Moreover, E2-treated NF-pBMSCs decreased in ${\beta}$-galactosidase activity but no influence on NM-pBMSCs. In E2-mediated differentiation capacity, E2 induced an increase in the osteogenic and chondrogenic abilities of both pBMSCs, but adipogenic ability may increased only in NF-pBMSCs. These results demonstrate that E2 could affect both genders of newborn donor-derived MSCs, but the regulatory role of E2 varies depending on gender-dependent characteristics even though the original newborn donors had not been affected by functional steroid hormones.

• Journal of Life Science
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• v.33 no.6
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• pp.463-470
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• 2023

Desmarestia tabacoides Okamura is a brown macroalgae that is found worldwide. Although several genera of Desmarestia have been reported as having anti-tumorigenic, anti-melanogenic, and photoprotective properties, the anti-inflammatory activity of D. tabacoides Okamura has not yet been evaluated. In this study, we analyzed the anti-inflammatory mechanisms of D. tabacoides Okamura ethanol extract (DTEE) via the inhibition of nitric oxide (NO) and prostaglandin (PG) E₂ production and the expression of their corresponding enzymes, inducible NO synthase (iNOS), and cyclooxygenase (COX)-2. In addition, their upstream signaling molecules were evaluated by Western blot analysis, such as nuclear factor (NF)-κB, mitogen-activated protein kinase (MAPK), and phosphoinositide-3-kinase (PI3K)/Akt, in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. The DTEE treatment significantly inhibited LPS-induced NO and PGE₂ production as well as the expression of their corresponding enzymes, iNOS, and COX-2 without cytotoxicity. The stimulated transcription factor NF-κB and upstream signaling molecules extracellular signal-regulated kinase (ERK), c-Jun NH₂-terminal kinase (JNK), and p38 were attenuated by the DTEE treatment, which was statistically significant, while Akt did not provide any inhibitory effect. Moreover, the DTEE treatment significantly mitigated the LPS-activated adaptor molecules, toll-like receptor 4 (TLR4), and myeloid differentiation primary response 88 (MyD88) in the RAW 264.7 cells. These results suggest that DTEE attenuates TLR4-mediated inflammatory responses by inhibiting NF-κB activation and suppressing MAPK phosphorylation in LPS-stimulated RAW 264.7 cells.

• BMB Reports
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• v.33 no.6
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• pp.454-462
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• 2000

Interleukin-4(IL-4) is known to be a major cytokine regulating immunoglobulin E(IgE) response by the induction of IgE production and type II IgE receptor(IgER II: CD23) expression. Recently, however, the role of neuroendocrine factors has been implicated in modulating the IgE response. Among various neuroendocrine growth factors, we investigated the effects of the insulin-like growth factor-1(IGF-1) since IL-4 and IGF-1 share common intracellular signaling molecules, such as the insulin receptor substrate-1/2(IRS-1/2) to induce a specific cellular response. In the human peripheral blood mononuclear cell (PBMC) cultures, IGF-1 was capable of inducing a substantial level of IgE production in a dose-dependent manner. It also noticeably upregulated the IL-4-induced or IL-4 plus anti-CD40-induced IgE production. Similarly, the IGF-1-induced IgE production was enhanced by IL-4 or anti-CD40 in an additive manner, which became saturated at high concentrations of IGF-1. Although IGF-1 alone did not induce IgER II (CD23) expression, it augmented the IL-4-induced surface CD23 expression in a manner similar to the action of anti-CD40. These results imply that IGF-1 is likely to utilize common signaling pathways with IL-4 and anti-CD40 to induce IgE and IgER II expression. In support of this notion, we observed that IGF-1 enhanced the IL-4-induced signal transducers and activators of transcription 6(STAT6) activation and independently induced $NF-{\kappa}B$ activation. Both of these bind to the IgE(C) or IgER II (CD23) promoters. Together, our data suggest that IL-4 and IGF-1 work cooperatively to activate STAT6 and $NF-{\kappa}B$. This leads to the subsequent binding of these transcription factors to the $C{\varepsilon}$ and CD23 promoters to enhance the expression of IgE and IgER II. The observed differential ability of IGF-1 on the induction of IgE vs. IgER II is discussed based on the different structure of the two promoters.