Non-cellular Systems Research Articles

Soluble CD147 regulates endostatin via its effects on the activities of MMP-9 and secreted proteasome 20S.

During progression of rheumatoid arthritis (RA), angiogenesis provides oxygen and nutrients for the cells' increased metabolic demands and number. To turn on angiogenesis, pro-angiogenic factors must outweigh anti-angiogenic factors. We have previously shown that CD147/extracellular matrix metalloproteinase inducer (EMMPRIN) can induce the expression of the pro-angiogenic factors vascular endothelial growth factor (VEGF) and matrix metallopeptidase 9 (MMP-9) in a co-culture of the human HT1080 fibrosarcoma and U937 monocytic-like cell lines. However, whether CD147 influences anti-angiogenic factors was not known. We now show that relative to single cultures, the co-culture of these cells not only enhanced pro-angiogenic factors but also decreased the anti-angiogenic factors endostatin and thrombospondin-1 (Tsp-1), generally increasing the angiogenic potential as measured by a wound assay. Using anti-CD147 antibody, CD147 small interfering RNA (siRNA), and recombinant CD147, we demonstrate that CD147 hormetically regulates the generation of endostatin but has no effect on Tsp-1. Since endostatin is cleaved from collagen XVIII (Col18A), we applied different protease inhibitors and established that MMP-9 and proteasome 20S, but not cathepsins, are responsible for endostatin generation. MMP-9 and proteasome 20S collaborate to synergistically enhance endostatin generation, and in a non-cellular system, CD147 enhanced MMP-9 activity and hormetically regulated proteasome 20S activity. Serum samples obtained from RA patients and healthy controls mostly corroborated these findings, indicating clinical relevance. Cumulatively, these findings suggest that secreted CD147 mediates a possibly allosteric effect on MMP-9 and proteasome 20S activities and can serve as a switch that turns angiogenesis on or off, depending on its ambient concentrations in the microenvironment.

DNA-Based Mechanical Sensors for Cell Applications

Cells constantly experience mechanical forces during growth and development. Increasing evidence suggests that mechanical forces can regulate cellular processes such as proliferation, migration, and differentiation. Therefore, developing new tools to measure and manipulate cellular mechanical forces is essential. DNA nanostructures, due to their simple design and high programmability, have been utilized to create various mechanical sensors and have become a key tool for studying mechanical information in both cellular and non-cellular systems. In this article, we review the development of DNA-based mechanical sensors and their applications in measuring mechanical forces in the extracellular matrix and cell–cell interactions and summarize the latest advances in monitoring and manipulating cellular morphology and function. We hope that this review can provide insights for the development of new mechanical nanodevices.

Exosomes derived from human umbilical cord mesenchymal stem cells (HUCMSC-EXO) regulate autophagy through AMPK-ULK1 signaling pathway to ameliorate diabetic cardiomyopathy

One of the main causes of severe diabetic heart failure and mortality is diabetic cardiomyopathy (DCM), a cardiovascular condition attributable to diabetes with a high incidence, a complicated and unexplained pathophysiology, and poor treatment results. Current findings have demonstrated that the onset of diabetic cardiomyopathy involves autophagy, inflammation, and mitochondrial damage. Myocardial autophagy behaves differently in different states,and one of the targets for the detection and treatment of cardiovascular illnesses like diabetic cardiomyopathy may be the control of autophagy. The role of human umbilical cord Mesenchymal stem cells-derived exosomes (HUCMSC-EXO) as a non-cellular system in the repair of cardiomyocytes, the evolution of diabetic cardiomyopathy and their cardioprotective effects are gradually being recognized. This study's objectives were to assess the therapeutic benefits of HUCMSC-EXO for diabetic cardiomyopathy and to look into their potential mechanisms of action. High-speed centrifugation was used to extract HUCMSC-EXO, and the shape of the exosomes was examined using transmission electron microscopy. Immunoblotting was used to determine the expression of CD9, CD63, and TSG101 molecules on the surface of the exosomes. A high-fat, high-sugar diet mixed with streptozotocin was used to build a rat model of type 2 diabetic cardiomyopathy. Cardiac function, ventricular wall thickness and cardiac histological changes were examined by cardiac ultrasound, serum BNP and histology. In cardiac myocytes, HUCMSC-EXO reduced the levels of autophagy-related protein expression. Additionally, immunoblotting supported our suspicion that this mechanism is strongly tied to the activation of the AMPK-ULK1 signaling pathway. So, we propose that it would be a good strategy to follow for treating diabetic cardiomyopathy. These findings offer both fresh concepts for building a model of diabetic cardiomyopathy and a creative theoretical framework for using HUCMSC-EXO to treat diabetic cardiomyopathy in a clinical setting.

Overriding native cell coordination enhances external programming of collective cell migration

As collective cell migration is essential in biological processes spanning development, healing, and cancer progression, methods to externally program cell migration are of great value. However, problems can arise if the external commands compete with strong, preexisting collective behaviors in the tissue or system. We investigate this problem by applying a potent external migratory cue-electrical stimulation and electrotaxis-to primary mouse skin monolayers where we can tune cell-cell adhesion strength to modulate endogenous collectivity. Monolayers with high cell-cell adhesion showed strong natural coordination and resisted electrotactic control, with this conflict actively damaging the leading edge of the tissue. However, reducing preexisting coordination in the tissue by specifically inhibiting E-cadherin-dependent cell-cell adhesion, either by disrupting the formation of cell-cell junctions with E-cadherin-specific antibodies or rapidly dismantling E-cadherin junctions with calcium chelators, significantly improved controllability. Finally, we applied this paradigm of weakening existing coordination to improve control and demonstrate accelerated wound closure in vitro. These results are in keeping with those from diverse, noncellular systems and confirm that endogenous collectivity should be considered as a key quantitative design variable when optimizing external control of collective migration.

SARS‐CoV‐2: pushing the E(nvelope)

SARS‐CoV‐2: pushing the E(nvelope)

Metabolic Profiles of New Unsymmetrical Bisacridine Antitumor Agents in Electrochemical and Enzymatic Noncellular Systems and in Tumor Cells.

New unsymmetrical bisacridines (UAs) demonstrated high activity not only against a set of tumor cell lines but also against human tumor xenografts in nude mice. Representative UA compounds, named C-2028, C-2045 and C-2053, were characterized in respect to their physicochemical properties and the following studies aimed to elucidate the role of metabolic transformations in UAs action. We demonstrated with phase I and phase II enzymes in vitro and in tumors cells that: (i) metabolic products generated by cytochrome P450 (P450), flavin monooxygenase (FMO) and UDP-glucuronosyltransferase (UGT) isoenzymes in noncellular systems retained the compound’s dimeric structures, (ii) the main transformation pathway is the nitro group reduction with P450 isoenzymes and the metabolism to N-oxide derivative with FMO1, (iii), the selected UGT1 isoenzymes participated in the glucuronidation of one compound, C-2045, the hydroxy derivative. Metabolism in tumor cells, HCT-116 and HT-29, of normal and higher UGT1A10 expression, respectively, also resulted in the glucuronidation of only C-2045 and the specific distribution of all compounds between the cell medium and cell extract was demonstrated. Moreover, P4503A4 activity was inhibited by C-2045 and C-2053, whereas C-2028 affected UGT1A and UGT2B action. The above conclusions indicate the optimal strategy for the balance among antitumor therapeutic efficacy and drug resistance in the future antitumor therapy.

Efficient Anticancer Effect on Choroidal Melanoma Cells Induced by Tanshinone IIA Photosensitization

Tanshinone IIA (TanIIA) has multiple biological functions and already been clinically used to treat many cardiovascular diseases. TanIIA is a photoactive molecule and can be excited by light to generate 3 TanIIA*. Generation of 3 TanIIA* by TanIIA photosensitization indicates that TanIIA may serve as a photosensitizer to bring photodynamic damage to organisms. Therefore, human choroidal melanoma MUM-2B cell was chosen as a superficial tumor model and the photodynamic effect of TanIIA on tumor cells was evaluated in this study. The results showed that TanIIA photosensitization could generate singlet oxygen in noncellular system. MTT, clone formation and wound-healing assays showed that the survival and migration of MUM-2B cells could be efficiently inhibited by TanIIA photosensitization. And then, laser confocal microscope and flow cytometry were used to try to elucidate related mechanism. It was found that TanIIA could pass through cellular membrane and preferably accumulate in nucleus. TanIIA photosensitization could efficiently induce cell apoptosis and necrosis, increase intracellular ROS levels, decrease mitochondria membrane potential, and lead to cell cycle arrest in G2/M phase. Our findings indicate that TanIIA photosensitization can exert remarkable toxicity on choroidal melanoma cells.

Enhanced Activity of P4503A4 and UGT1A10 Induced by Acridinone Derivatives C-1305 and C-1311 in MCF-7 and HCT116 Cancer Cells: Consequences for the Drugs' Cytotoxicity, Metabolism and Cellular Response.

Activity modulation of drug metabolism enzymes can change the biotransformation of chemotherapeutics and cellular responses induced by them. As a result, drug-drug interactions can be modified. Acridinone derivatives, represented here by C-1305 and C-1311, are potent anticancer drugs. Previous studies in non-cellular systems showed that they are mechanism-based inhibitors of cytochrome P4503A4 and undergo glucuronidation via UDP-glucuronosyltranspherase 1A10 isoenzyme (UGT1A10). Therefore, we investigated the potency of these compounds to modulate P4503A4 and UGT1A10 activity in breast MCF-7 and colon HCT116 cancer cells and their influence on cytotoxicity and cellular response in cells with different expression levels of studied isoenzymes. We show that C-1305 and C-1311 are inducers of not only P4503A4 but also UGT1A10 activity. MCF-7 and HCT116 cells with high P4503A4 activity are more sensitive to acridinone derivatives and undergo apoptosis/necrosis to a greater extent. UGT1A10 was demonstrated to be responsible for C-1305 and C-1311 glucuronidation in cancer cells and glucuronide products were excreted outside the cell very fast. Finally, we show that glucuronidation of C-1305 antitumor agent enhances its pro-apoptotic properties in HCT116 cells, while the cytotoxicity and cellular response induced by C-1311 did not change after drug glucuronidation in both cell lines.

New Unsymmetrical Bisacridine Derivatives Noncovalently Attached to Quaternary Quantum Dots Improve Cancer Therapy by Enhancing Cytotoxicity toward Cancer Cells and Protecting Normal Cells.

The use of nanoparticles for the controlled drug delivery to cells has emerged as a good alternative to traditional systemic delivery. Quantum dots (QDs) offer potentially invaluable societal benefits such as drug targeting and in vivo biomedical imaging. In contrast, QDs may also pose risks to human health and the environment under certain conditions. Here, we demonstrated that a unique combination of nanocrystals core components (Ag-In-Zn-S) would eliminate the toxicity problem and increase their biomedical applications. The alloyed quaternary nanocrystals Ag-In-Zn-S (QDgreen, Ag1.0In1.2Zn5.6S9.4; QDred, Ag1.0In1.0Zn1.0S3.5) were used to transport new unsymmetrical bisacridine derivatives (UAs, C-2028 and C-2045) into lung H460 and colon HCT116 cancer cells for improving the cytotoxic and antitumor action of these compounds. UAs were coupled with QD through physical adsorption. The obtained results clearly indicate that the synthesized nanoconjugates exhibited higher cytotoxic activity than unbound compounds, especially toward lung H460 cancer cells. Importantly, unsymmetrical bisacridines noncovalently attached to QD strongly protect normal cells from the drug action. It is worth pointing out that QDgreen or QDred without UAs did not influence the growth of cancer and normal cells, which is consistent with in vivo results. In noncellular systems, at pH 5.5 and 4.0, which relates to the conditions of endosomes and lysosomes, the UAs were released from QD-UAs nanoconjugates. An increase of total lysosomes content was observed in H460 cells treated with QDs-UAs which can affect the release of the UAs from the conjugates. Moreover, confocal laser scanning microscopy analyses revealed that QD-UAs nanoconjugates enter H460 cells more efficiently than to HCT116 and normal cells, which may be the reason for their higher cytotoxicity against lung cancer. Summarizing, the noncovalent attachment of UAs to QDs increases the therapeutic efficiency of UAs by improving cytotoxicity toward lung H460 cancer cells and having protecting effects on normal cells.

Fucose-Galactose Polymers Inhibit Cholera Toxin Binding to Fucosylated Structures and Galactose-Dependent Intoxication of Human Enteroids.

A promising strategy to limit cholera severity involves blockers mimicking the canonical cholera toxin ligand (CT) ganglioside GM1. However, to date the efficacies of most of these blockers have been evaluated in noncellular systems that lack ligands other than GM1. Importantly, the CT B subunit (CTB) has a noncanonical site that binds fucosylated structures, which in contrast to GM1 are highly expressed in the human intestine. Here we evaluate the capacity of norbornene polymers displaying galactose and/or fucose to block CTB binding to immobilized protein-linked glycan structures and also to primary human and murine small intestine epithelial cells (SI ECs). We show that the binding of CTB to human SI ECs is largely dependent on the noncanonical binding site, and interference with the canonical site has a limited effect while the opposite is observed with murine SI ECs. The galactose–fucose polymer blocks binding to fucosylated glycans but not to GM1. However, the preincubation of CT with the galactose–fucose polymer only partially blocks toxic effects on cultured human enteroid cells, while preincubation with GM1 completely blocks CT-mediated secretion. Our results support a model whereby the binding of fucose to the noncanonical site places CT in close proximity to scarcely expressed galactose receptors such as GM1 to enable binding via the canonical site leading to CT internalization and intoxication. Our finding also highlights the importance of complementing CTB binding studies with functional intoxication studies when assessing the efficacy inhibitors of CT.

Modified state diagrams of cellular and noncellular food model systems: Experimental data and mathematical modeling

The state diagram is an interesting approach to assess the stability of food products. In addition, the cellular structure could also have an impact on the behavior of food products during processing and storage. In this study, potato and carrot (cellular structure) and two gel food systems made from water–agar–maltodextrin (noncellular structure) were used to obtain experimental data of aw and Tg as a function of water content during drying. The Guggenheim–Anderson-de Boer (GAB), Flory–Huggins, Gordon–Taylor, and Khalloufi–Ratti models were assessed by comparing them to the experimental data. The results obtained showed that these mathematical expressions can be used to capture the experimental data profiles with acceptable accuracy. Both GAB and Khalloufi–Ratti models were used as tools to build the modified state diagrams of the four products investigated in this study. As the number of the samples studied was limited, it was not possible to establish whether cellular structures have a larger impact on Tg than other parameter such as the chemical composition of the products.

Determination of Oxidative Potential Caused by Brake Wear Debris in Non-Cellular Systems.

Wear debris from automotive brake systems represents a major source of non-exhaust emissions from road traffic and its production increases with number of cars worldwide. However, impact of brake wear debris on the environment and organisms is still not clear. One of the most possible ways by which these particles may affect living organisms is oxidative stress. Production of reactive oxidative species may cause damage of basic cell components, lipids, proteins, etc. Aim of this study is to perform characterization of airborne and nonairborne fractions of brake wear debris generated during standard dynamometer tests and evaluation of its potential to induce oxidative stress via lipid peroxidation and carbonylation of proteins in non-cellular system. Elemental and phase composition were determined by scanning electron microscopy, Raman microspectroscopy, and X-ray powder diffraction analysis. Carbon in amorphous form and graphite, copper, and iron in form of oxides were identified as major components in both studied fractions. Characteristic size of studied wear particles was evaluated by dynamic light scattering. Both airborne and nonairborne samples showed ability to induce oxidative stress which results from determination of carbonylated proteins.

Evaluation of In Vitro Antioxidant Activity of the Water Extract Obtained from Dried Pine Needle (Pinus densiflora).

Antioxidant activities of water extracts obtained from dried pine needle (Pinus densiflora) were measured at 0, 4, 20, 100, 500, 1,000, and 1,200 ppm and compared with those of phenolic compounds of butylated hydroxyanisole, butylated hydroxytoluene, tert-butylhydroquinone, ferulic acid, and α-tocopherol. The activity was determined as the ability to scavenge 1,1-diphenyl-2-picrylhydrazyl radical and hydrogen peroxide, reductive power, and inhibition of lipid peroxidation in a linoleic acid system using the ferric thiocyanate method and thiobarbituric acid method, respectively. Pine needle water extract (PNWE) exhibited antioxidant activity in a concentration-dependent mode at the same parameters mentioned above, and a significant difference (P<0.05) was observed at 1,000 ppm. The protective activity of PNWE as a potent antioxidant in a non-cellular system was compared with that of phenolics at 150.67 μg/mL in the two assays using biological cellular systems, namely 2,2′-azobis(2-amidinopropane) dihydrochloride-initiated hemolysis and Fe2+-induced lipid peroxidation, using rat red blood cells and rat brain homogenate, respectively. The PNWE showed a strong power comparable to those of commercial phenolic compounds in biological systems. These results indicated that the protective activity of PNWE could be due to the presence of naturally-occurring phenolic compounds, which act as potent in vitro antioxidants in both non-cellular and cellular systems.

Modulation of UDP-glucuronidation by acridinone antitumor agents C-1305 and C-1311 in HepG2 and HT29 cell lines, despite slight impact in noncellular systems.

Among the studied antitumor acridinone derivatives developed in our laboratory, 5-dimethylaminopropylamino-8-hydroxytriazoloacridinone (C-1305) and 5-diethylaminoethylamino-8-hydroxyimidazoacridinone (C-1311) exhibited cytotoxic and antitumor properties against several cancer types and were selected to be evaluated in preclinical and early-phase clinical trials. In the present work, we investigated the impact of C-1305 and C-1311 on UDP-glucuronosyltransferase (UGT) activity. Enzyme activity modulation was studied using HPLC by analyzing standard UGT substrate metabolism in the presence and absence of antitumor drugs. The investigations were performed in two model systems: (i) under noncellular conditions, including human liver microsomes (HLM) and recombinant UGT1A1, 1A9 and 1A10 isoenzymes and (ii) in tumor cells. There was observed a slight impact of studied drugs on enzyme activity. Only UGT1A1 action was altered by both compounds. The modulatory effects of UGT activity in cellular systems depended on the tumor cell type. In the case of HepG2, C-1305 and C-1311 strongly induced UGT activity, particularly for C-1311, at concentrations significantly lower than the EC50. This effect contradicted irinotecan mediated UGT inhibition. HT29 colon tumor cells were less sensitive than HepG2 to enzyme modulation in the presence of the studied compounds, particularly C-1305, where enzymatic inhibition similar to that of irinotecan was observed. The results demonstrated that UGT activity modulation should be expected in the case of antitumor therapy with C-1305 or/and C-1311. Analysis of the results indicated that these modulations would occur via cellular regulatory pathways not by direct drug-enzyme interactions.

Revisiting blood-brain barrier: A chromatographic approach

Drugs designed to reach a pharmacological CNS target must be effectively transported across the blood-brain barrier (BBB), a thin monolayer of endothelial cells tightly attached together between the blood and the brain parenchyma. Because of the lipidic nature of the BBB, several physicochemical partition models have been studied as surrogates for the passive permeation of potential drug candidates across the BBB (octanol-water, alkane-water, PAMPA...). In the last years, biopartition chromatography is gaining importance as a noncellular system for the estimation of biological properties in early stages of drug development. Microemulsions (ME) are suitable mobile phases, because of their ease of formulation, stability and adjustability to a large number of compositions mimicking biological structures. In the present work, several microemulsion liquid chromatographic (MELC) systems have been characterized by means of the Abraham’s solvation parameter model, in order to assess their suitability as BBB distribution or permeability surrogates. In terms of similarity between BBB and MELC systems (dispersion forces arising from solute non-bonded electrons, dipolarity/polarizability, hydrogen-bond acidity and basicity, and molecular volume), the passive permeability surface area product (log PS) for neutral (including zwitterions), fully and partially ionized drugs was found to be well correlated with the ME made of 3.3% SDS (w/v; surfactant) 0.8% heptane (w/v; oil phase) and 6.6% 1-butanol (w/v; co-surfactant) in 50mM aqueous phosphate buffer, pH 7.4.

Intracellular ATP in balance of pro- and anti-inflammatory cytokines in adipose tissue with and without tissue expansion.

OBJECTIVESTo understand the mechanism of white fat expansion in the presence of inflammation, we examined the balance of pro- and anti-inflammatory cytokines in epididymal fat during weight gain in DIO mice.METHODSThe pro- and anti-inflammatory cytokines were examined in white fat of diet-induced obese mice and lean mice. The mechanism of gene expression was investigated with a focus on intracellular ATP (iATP). ATP activity was tested in cellular and non-cellular systems in activation of serine kinases (IKKβ, JNK and ERK).RESULTSThe pro- (TNF-α, IL-1β, IL-6, MCP-1, IFN-γ and OPN) and the anti-inflammatory cytokines (IL-10, IL-1Ra, IL-13, sTNFR2, PEDF and adiponectin) were increased at the same time during the weight gain. The balance was observed even in the absence of tissue expansion upon feeding in lean and obese mice. The iATP levels were positively associated with the cytokine elevation in the adipose tissue. In macrophages, induction of iATP with lauric acid stimulated the expression. Inhibition of iATP with β-oxidation inhibitor (Etomoxir) or mitochondrial uncoupler (2,4-dinitrophenol, DNP) suppressed the expression. ATP exhibited an activity in the activation of inflammatory kinases (IKKβ, JNK and ERK) in the living cells and cell lysate. The kinase activation was blocked in the cells by ATP inhibition.CONCLUSIONSThe data suggest that the pro- and anti-inflammatory cytokines are dynamically balanced in the white adipose tissue by iATP.

Coupling carboxylic acid reductase to inorganic pyrophosphatase enhances cell-free in vitro aldehyde biosynthesis

Carboxylic acid reductases (CARs) have been harnessed in metabolic pathways to produce aldehydes in engineered organisms. However, desired aldehyde products inhibit cell growth and limit product titers currently achievable from fermentative processes. Aldehyde toxicity can be entirely circumvented by performing aldehyde biosynthesis in non-cellular systems. Use of purified CARs for preparative-scale aldehyde synthesis has been limited by in vitro turnover of model CARs, such as CarNi from Nocardia iowensis, despite robust conversion of substrates associated with expression in heterologous hosts such as E. coli and yeast. In this study, we report that in vitro activity of CarNi is inhibited by formation of the co-product pyrophosphate, and that pairing of an inorganic pyrophosphatase (PpaEc) with CarNi substantially improves the rate and yield of aldehyde biosynthesis. We demonstrate that, in the presence of PpaEc, Michaelis–Menten kinetic models based on initial rate measurements accurately predict CarNi kinetics within an in vitro pathway over longer timescales. We rationalize our novel observations for CarNi by examining previously posed arguments for pyrophosphate hydrolysis made in the context of other adenylate-forming enzymes. Overall, our findings may aid in increasing adoption of CARs for cell-free in vitro aldehyde biosynthetic processes.

Superoxide Anion Radical: Generation and Detection in Cellular and Non-Cellular Systems.

The production of superoxide anion radical (O2•(-)) is essential for the life of aerobic organisms. This free radical acts as a signaling molecule, regulating numerous biological processes including apoptosis, aging, and senescence. Nevertheless, when overproduction of O2•(-) occurs and/or antioxidant defences are deficient, oxidative stress may develop, damaging important biomolecules and altering their physiological function. These effects have been associated to the development of several diseases. Scavenging of O2•(-) has been used as a hallmark to test the antioxidant capacity of several types of compounds in cellular and non-cellular systems. However, despite the pathophysiological importance of O2•(-), the information about its endogenous and/or chemical generation and detection is dispersed and there are no reports that concisely cover the information in an integrated form. This gap can explain the limitations attributed to the currently used systems, namely in what concerns the selectivity, specificity and validation. This review attempts to provide a critical assessment of the available O2•(-) generating and detection, both in endogenous and chemical systems, scrutinizing its advantages and limitations in order to facilitate the choice and implementation of the O2•(-) generator and/or detection method that better fits the researchers' objectives.

쪽의 항산화 및 항염증 활성에 대한 연구

Objectives : Persicaria tinctoria belongs to the Polygonaceae family and it has been used as the natural dye traditionally. Also, it is well known that the Persicaria tinctoria is used for treating the following symptoms such as fever, inflammation and edema. The purpose of this study is to investigate the effective source of antioxidants and anti-inflammatory agent from various parts of Persicaria tinctoria. Methods : We investigated the antioxidative and anti-inflammatory properties of the Persicaria tinctoria extracts. Antioxidant activities were measured by 1,1-diphenyl-2picrylhydrazyl (DPPH), 2, 2'-Azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt (ABTS) radical scavenging activity, Fe chelating activity and Reducing power of Persicaria tinctoria extracts. And its inhibitory effect against oxidative DNA damage was evaluated in non-cellular system using φX-174 RF I plasmin DNA. The anti-inflammatory effect of Persicaria tinctoria was measured by using the inhibitory efficacy for the amount of nitric-oxide (NO) produced in LPS induced RAW264.7 cells. Results : The extracts from stem part showed better DPPH scavenging activity compared to those of the leaf and root extracts. Their IC50s were measured as 7.17, 144.40 and 165.07 ug/ml, respectively. These results were similar to that of ABTS radical scavenging assay and reducing power. Also, Persicaria tinctoria showed the protective effects of DNA damage against oxidative stress and anti-inflammatory effect by suppression of NO production in LPS induced RAW264.7 cells. Conclusions : These results showed that various parts of Persicaria tinctoria can be used as an effective source of antioxidants and anti-inflammatory agents via antioxidative activities and anti-inflammatory effect.

Study on Antioxidant and Anti-inflammatory Activities of Persicaria tinctoria

Objectives : Persicaria tinctoria belongs to the Polygonaceae family and it has been used as the natural dye traditionally. Also, it is well known that the Persicaria tinctoria is used for treating the following symptoms such as fever, inflammation and edema. The purpose of this study is to investigate the effective source of antioxidants and anti-inflammatory agent from various parts of Persicaria tinctoria. Methods : We investigated the antioxidative and anti-inflammatory properties of the Persicaria tinctoria extracts. Antioxidant activities were measured by 1,1-diphenyl-2picrylhydrazyl (DPPH), 2, 2'-Azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt (ABTS) radical scavenging activity, Fe chelating activity and Reducing power of Persicaria tinctoria extracts. And its inhibitory effect against oxidative DNA damage was evaluated in non-cellular system using φX-174 RF I plasmin DNA. The anti-inflammatory effect of Persicaria tinctoria was measured by using the inhibitory efficacy for the amount of nitric-oxide (NO) produced in LPS induced RAW264.7 cells. Results : The extracts from stem part showed better DPPH scavenging activity compared to those of the leaf and root extracts. Their IC50s were measured as 7.17, 144.40 and 165.07 ug/ml, respectively. These results were similar to that of ABTS radical scavenging assay and reducing power. Also, Persicaria tinctoria showed the protective effects of DNA damage against oxidative stress and anti-inflammatory effect by suppression of NO production in LPS induced RAW264.7 cells. Conclusions : These results showed that various parts of Persicaria tinctoria can be used as an effective source of antioxidants and anti-inflammatory agents via antioxidative activities and anti-inflammatory effect.