Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 10 de 10
Filter
Add more filters










Publication year range
1.
Membranes (Basel) ; 13(6)2023 Jun 12.
Article in English | MEDLINE | ID: mdl-37367799

ABSTRACT

Acetaldehyde (CH3CHO) in the atmosphere is associated with adverse health effects. Among the various options for use in removing CH3CHO, adsorption is often employed because of its convenient application and economical processes, particularly when using activated carbon. In previous studies, the surface of activated carbon has been modified with amines to remove CH3CHO from the atmosphere via adsorption. However, these materials are toxic and can have harmful effects on humans when the modified activated carbon is used in air-purifier filters. Therefore, in this study, a customized bead-type activated carbon (BAC) with surface modification options via amination was evaluated for removing CH3CHO. Various amounts of non-toxic piperazine or piperazine/nitric acid were used in amination. Chemical and physical analyses of the surface-modified BAC samples were performed using Brunauer-Emmett-Teller measurements, elemental analyses, and Fourier transform infrared and X-ray photoelectron spectroscopy. The chemical structures on the surfaces of the modified BACs were analyzed in detail using X-ray absorption spectroscopy. The amine and carboxylic acid groups on the surfaces of the modified BACs are critical in CH3CHO adsorption. Notably, piperazine amination decreased the pore size and volume of the modified BAC, but piperazine/nitric acid impregnation maintained the pore size and volume of the modified BAC. In terms of CH3CHO adsorption, piperazine/nitric acid impregnation resulted in a superior performance, with greater chemical adsorption. The linkages between the amine and carboxylic acid groups may function differently in piperazine amination and piperazine/nitric acid treatment.

2.
J Infect Dis ; 215(10): 1608-1618, 2017 05 15.
Article in English | MEDLINE | ID: mdl-28368519

ABSTRACT

Background: Countervailing anti-inflammatory response and immunosuppression can cause death in late sepsis. Depletion and dysfunction of T cells are critical for developing sepsis-induced immunosuppression. Heme oxygenase-1 (HO-1) has a regulatory effect on differentiation and function of T cells and anti-inflammatory properties. We therefore investigated the immunosuppressive role of HO-1 in sepsis with a focus on its effects on helper T-cell (Th) differentiation and regulatory T cells (Treg). Methods: Sepsis was induced by cecal ligation and puncture (CLP). Mice were intraperitoneally injected with zinc protoporphyrin (ZnPP; 25 mg/kg), an HO-1 inhibitor, or hemin (20 mg/kg), an HO-1 inducer, at 24 and 36 hours post-CLP. Splenocytes were isolated 48 hours post-CLP. Mice were intranasally infected with Pseudomonas aeruginosa 4 days post-CLP as a secondary pneumonia infection model. Results: ZnPP improved survival and bacterial clearance, whereas hemin had the opposite effect in septic mice. CLP induced lymphocyte apoptosis and a proinflammatory Th1 to anti-inflammatory Th2 shift, which was attenuated by ZnPP. ZnPP attenuated the CLP-induced Treg population and protein expression of inhibitory costimulatory molecules. Furthermore, ZnPP improved survival in the secondary pneumonia infection model. Conclusions: Our findings suggest that HO-1 overexpression contributes to sepsis-induced immunosuppression during late phase sepsis by promoting Th2 polarization and Treg function.


Subject(s)
Apoptosis/immunology , Heme Oxygenase-1/immunology , Sepsis/immunology , T-Lymphocytes, Helper-Inducer/immunology , T-Lymphocytes, Regulatory/immunology , Animals , Apoptosis/drug effects , Heme Oxygenase-1/analysis , Heme Oxygenase-1/antagonists & inhibitors , Heme Oxygenase-1/metabolism , Immunocompromised Host , Mice , Mice, Inbred C57BL , Protoporphyrins/pharmacology , Pseudomonas Infections/immunology , Pseudomonas Infections/physiopathology , Pseudomonas aeruginosa/immunology , Sepsis/physiopathology , T-Lymphocytes, Helper-Inducer/drug effects , T-Lymphocytes, Regulatory/drug effects
3.
J Ethnopharmacol ; 155(1): 256-66, 2014 Aug 08.
Article in English | MEDLINE | ID: mdl-24862492

ABSTRACT

ETHNOPHARMACOLOGICAL RELEVANCE: Lonicera japonica Thunberg is a traditional herbal medicine widely used in East Asia as an anti-bacterial, anti-inflammatory, and antiviral agent. This study was designed to investigate the effects of HS-23, ethanol extract of the dried flower buds of Lonicera japonica, in experimental models of sepsis and elucidate the mechanisms of action of HS-23. MATERIALS AND METHODS: Male ICR mice were intravenously administered HS-23 (20 and 40 mg/kg) for 0 (immediately) and 24 h after cecal ligation and puncture (CLP) for survival tests, and HS-23 (40 mg/kg) immediately after CLP for biochemical assays. RESULTS: HS-23 improved sepsis-induced mortality, enhanced bacterial clearance, and attenuated multiple organ failure. The mechanisms of action of HS-23 included attenuation of increased toll-like receptor (TLR)4 protein and mRNA expression. HS-23 suppressed sepsis-induced increases in protein expression of myeloid differentiation primary response protein 88, p38 and c-Jun N-terminal kinase in both liver and lung, as well as TIR-domain-containing adapter-inducing interferon-ß and interferon regulatory transcription factor 3 protein expression in liver. CONCLUSION: The results of this study revealed that HS-23 attenuated sepsis through suppression of TLR signaling pathways. Therefore, our findings suggest that HS-23 might be useful as a potential therapeutic agent for treatment of sepsis.


Subject(s)
Lonicera/chemistry , Plant Extracts/pharmacology , Sepsis/drug therapy , Toll-Like Receptor 4/metabolism , Animals , Disease Models, Animal , Dose-Response Relationship, Drug , Liver/drug effects , Liver/metabolism , Lung/drug effects , Lung/metabolism , Male , Mice , Mice, Inbred ICR , Multiple Organ Failure/etiology , Multiple Organ Failure/prevention & control , Plant Extracts/administration & dosage , Plant Extracts/isolation & purification , RNA, Messenger/metabolism , Sepsis/mortality , Signal Transduction/drug effects
4.
Br J Pharmacol ; 169(6): 1404-16, 2013 Jul.
Article in English | MEDLINE | ID: mdl-23647130

ABSTRACT

BACKGROUND AND PURPOSE: PPAR-γ has been reported to be a protective regulator in ischaemia/reperfusion (I/R) injury. The receptor for advanced glycation end-products (RAGE) plays a major role in the innate immune response, and its expression is associated with PPAR-γ activation. Several angiotensin receptor blockers possess partial agonist activities towards PPAR-γ. Therefore, this study investigated the action of losartan, particularly with regard to PPAR-γ activation and RAGE signalling pathways during hepatic I/R. EXPERIMENTAL APPROACH: Mice were subjected to 60 min of ischaemia followed by 6 h of reperfusion. Losartan (0.1, 1, 3 and 10 mg · kg⁻¹) was administered 1 h prior to ischaemia and immediately before reperfusion. GW9662, a PPAR-γ antagonist, was administered 30 min prior to first pretreatment with losartan. KEY RESULTS: Losartan enhanced the DNA-binding activity of PPAR-γ in I/R. Losartan attenuated the increased serum alanine aminotransferase activity, TNF-α and IL-6 levels, and nuclear concentrations of NF-κB in I/R. GW9662 reversed these beneficial effects. Losartan caused a decrease in apoptosis as assessed by TUNEL assay, in release of cytochrome c and in cleavage of caspase-3, and these effects were abolished by GW9662 administration. Losartan attenuated not only I/R-induced RAGE overexpression, but also its downstream early growth response protein-1-dependent macrophage inflammatory protein 2 level; phosphorylation of p38, ERK and JNK; and subsequent c-Jun phosphorylation. GW9662 reversed these effects of losartan administration. CONCLUSIONS AND IMPLICATIONS: Our findings suggest that losartan ameliorates I/R-induced liver damage through PPAR-γ activation and down-regulation of the RAGE signalling pathway.


Subject(s)
Angiotensin II Type 1 Receptor Blockers/therapeutic use , Down-Regulation/drug effects , Liver/drug effects , Losartan/therapeutic use , PPAR gamma/agonists , Receptors, Immunologic/antagonists & inhibitors , Reperfusion Injury/prevention & control , Angiotensin II Type 1 Receptor Blockers/administration & dosage , Angiotensin II Type 1 Receptor Blockers/antagonists & inhibitors , Anilides/pharmacology , Animals , Apoptosis/drug effects , Cell Nucleus/drug effects , Cell Nucleus/metabolism , Cytokines/antagonists & inhibitors , Cytokines/blood , Dose-Response Relationship, Drug , Electrophoretic Mobility Shift Assay , Gene Expression Regulation/drug effects , Gene Silencing , Liver/blood supply , Liver/metabolism , Liver/physiopathology , Losartan/administration & dosage , Losartan/antagonists & inhibitors , MAP Kinase Signaling System/drug effects , Male , Mice , Mice, Inbred C57BL , PPAR gamma/antagonists & inhibitors , PPAR gamma/metabolism , Protective Agents/administration & dosage , Protective Agents/chemistry , Protective Agents/therapeutic use , Protein Transport/drug effects , Random Allocation , Receptor for Advanced Glycation End Products , Receptors, Immunologic/genetics , Receptors, Immunologic/metabolism , Reperfusion Injury/metabolism , Reperfusion Injury/physiopathology
5.
Mol Med ; 18: 1437-48, 2013 Jan 22.
Article in English | MEDLINE | ID: mdl-23168580

ABSTRACT

Sepsis is a complex, multifactorial, rapidly progressive disease characterized by an overwhelming activation of the immune system and the countervailing antiinflammatory response. In the current study in murine peritoneal macrophages, chlorogenic acid suppressed endotoxin-induced high mobility group box 1 (HMGB1) release in a concentration-dependent manner. Administration of chlorogenic acid also attenuated systemic HMGB1 accumulation in vivo and prevented mortality induced by endotoxemia and polymicrobial sepsis. The mechanisms of action of chlorogenic acid included attenuation of the increase in toll-like receptor (TLR)-4 expression and suppression of sepsis-induced signaling pathways, such as c-Jun NH2-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-κB, which are critical for cytokine release. The protection conferred by chlorogenic acid was achieved through modulation of cytokine and chemokine release, suppression of immune cell apoptosis and augmentation of bacterial elimination. Chlorogenic acid warrants further evaluation as a potential therapeutic agent for the treatment of sepsis and other potentially fatal systemic inflammatory disorders.


Subject(s)
Chlorogenic Acid/pharmacology , Chlorogenic Acid/therapeutic use , HMGB1 Protein/metabolism , Host-Pathogen Interactions/immunology , Immunity/drug effects , Sepsis/drug therapy , Sepsis/immunology , Animals , Apoptosis/drug effects , Cecum/drug effects , Cecum/pathology , Chemokines/metabolism , Chlorogenic Acid/administration & dosage , Endotoxemia/complications , Endotoxemia/drug therapy , Endotoxemia/microbiology , Endotoxemia/prevention & control , Host-Pathogen Interactions/drug effects , Inflammation/complications , Inflammation/metabolism , Inflammation/pathology , Intercellular Adhesion Molecule-1/metabolism , Ligation , Lipopolysaccharides , Macrophages, Peritoneal/drug effects , Macrophages, Peritoneal/metabolism , Male , Mice , Punctures , Sepsis/complications , Sepsis/microbiology , Signal Transduction/drug effects , Signal Transduction/immunology , Survival Analysis , Toll-Like Receptor 4/metabolism
6.
Food Chem Toxicol ; 50(7): 2335-41, 2012 Jul.
Article in English | MEDLINE | ID: mdl-22525864

ABSTRACT

This study examined the hepatoprotective effects of Agrimonia eupatoria water extract (AE) against chronic ethanol-induced liver injury. Rats were fed a Lieber-DeCarli liquid diet for 8 weeks. Animals were treated orally with AE at 10, 30, 100, and 300 mg/kg/day. After chronic consumption of ethanol, serum aminotransferase activities and pro-inflammatory cytokines markedly increased, and those increases were attenuated by AE. The cytochrome P450 2E1 activity and lipid peroxidation increased after chronic ethanol consumption, while reduced glutathione concentration decreased. Those changes were attenuated by AE. Chronic ethanol consumption increased the levels of Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 protein expression, inducible nitric oxide synthase and cyclooxygenase-2 protein and mRNA expression, and nuclear translocation of nuclear factor-kappa B, which was attenuated by AE. Our results suggest that AE ameliorates chronic ethanol-induced liver injury, and that protection is likely due to the suppression of oxidative stress and TLR-mediated inflammatory signaling.


Subject(s)
Agrimonia/chemistry , Ethanol/toxicity , Liver Diseases, Alcoholic/prevention & control , Plant Extracts/pharmacology , Animals , Base Sequence , Body Weight , Cytochrome P-450 CYP2E1/metabolism , Cytokines/blood , DNA Primers , Dose-Response Relationship, Drug , Inflammation Mediators/blood , Lipid Peroxidation , Male , NF-kappa B/metabolism , Rats , Rats, Sprague-Dawley , Reverse Transcriptase Polymerase Chain Reaction , Toll-Like Receptor 4/metabolism , Transaminases/blood
7.
Mol Med ; 18: 455-65, 2012 May 09.
Article in English | MEDLINE | ID: mdl-22252713

ABSTRACT

The pathogenesis of sepsis is characterized by overwhelming inflammatory responses that lead to tissue damage and organ failure. Toll-like receptor (TLR) signaling is crucial for induction of hyperinflammatory responses and tissue injury during sepsis. Genipin, an aglycon of geniposide, has antiinflammatory and antimicrobial activities. The purpose of this study was to test the hypothesis that genipin reduces multiple organ dysfunction and mortality during sepsis through inhibition of TLR signaling. Male ICR were subjected to sepsis by cecal ligation and puncture (CLP) or endotoxemia by lipopolysaccharide (LPS). Various doses of genipin (1, 2.5 and 5 mg/kg) or a vehicle were administered intravenously immediately after CLP or intraperitoneally after LPS treatment. In another set of survival tests, mice were treated with 2.5 mg/kg of genipin 0 and 24 h after CLP. Genipin was found to improve survival and to attenuate multiple organ dysfunction. Genipin attenuated production of proinflammatory cytokines and release of high-mobility group box 1 (HMGB1). Genipin prevented TLR2 and TLR4, myeloid differentiation factor 88 and the Toll/interleukin-1 receptor domain-containing adaptor protein, inducing interferon-ß overexpression. Phosphorylation of mitogen-activated protein kinases and interferon regulatory factor 3 and translocation of nuclear factor (NF)-κB were prevented by genipin. Moreover, genipin attenuated increases in serum tumor necrosis factor-α and HMGB1 in LPS-induced endotoxemia. Pam3CSK4- and LPS-mediated production of nitrites and proinflammatory cytokines was suppressed by genipin in RAW264.7 cells. Genipin attenuated mortality and organ injuries during sepsis through interference with TLR signaling. Therefore, genipin might be useful as a potential therapeutic agent for treatment of sepsis.


Subject(s)
Anti-Inflammatory Agents/therapeutic use , Iridoids/therapeutic use , Sepsis/drug therapy , Toll-Like Receptor 2/antagonists & inhibitors , Toll-Like Receptor 4/antagonists & inhibitors , Adaptor Proteins, Vesicular Transport/metabolism , Animals , Anti-Inflammatory Agents/pharmacology , Cell Line , Cell Survival/drug effects , Cytokines/blood , HMGB1 Protein/blood , Iridoids/pharmacology , Liver/drug effects , Liver/metabolism , Liver/pathology , Lung/drug effects , Lung/metabolism , Lung/pathology , Male , Mice , Mice, Inbred ICR , Mitogen-Activated Protein Kinases/metabolism , Myeloid Differentiation Factor 88/metabolism , Nitrites/metabolism , Sepsis/metabolism , Toll-Like Receptor 2/metabolism , Toll-Like Receptor 4/metabolism
8.
Exp Biol Med (Maywood) ; 237(1): 83-92, 2012 Jan.
Article in English | MEDLINE | ID: mdl-22185916

ABSTRACT

This study was designed to investigate the hepatoprotective effects of magnesium chenoursodeoxycholic acid (Mg-CUD), a magnesium trihydrate salt of ursodeoxycholic acid and chenodeoxycholic acid, in carbon tetrachloride (CCl(4))-induced liver fibrosis in rats. Rats were treated with CCl(4) dissolved in olive oil (0.5 mL/kg, twice a week) intraperitoneally for eight weeks. Mg-CUD was administered orally at 15.625, 31.25, 62.5 and 125 mg/kg once a day. Chronic CCl(4) administration induced increases in serum transforming growth factor-ß1, hepatic hydroxyproline content and serum alanine aminotransferase activity. Mg-CUD attenuated these increases. The levels of α-smooth muscle actin protein and mRNA expression were increased by chronic CCl(4) exposure and Mg-CUD attenuated these increases. Mg-CUD suppressed increases in matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-1 mRNA expression and elevation of oxidative stresses by attenuating lipid peroxidation and enhancing reduced glutathione/oxidized glutathione ratio. The overexpression of toll-like receptor 4 and increased nuclear translocation of nuclear factor-κB and phosphorylated c-Jun, a component of activator protein 1, were suppressed by Mg-CUD. Furthermore, CCl(4) increased the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-10 and cyclooxygenase (COX)-2. Mg-CUD attenuated the levels of TNF-α, IL-6 and COX-2, while it augmented the level of IL-10. Our results suggest that Mg-CUD may prevent liver fibrosis by modulating collagen accumulation and inflammatory signaling pathways.


Subject(s)
Carbon Tetrachloride Poisoning/drug therapy , Liver Cirrhosis/drug therapy , Organometallic Compounds/pharmacology , Actins/biosynthesis , Alanine Transaminase/biosynthesis , Alanine Transaminase/blood , Animals , Carbon Tetrachloride , Cyclooxygenase 2/biosynthesis , Cyclooxygenase 2/drug effects , Glutathione/metabolism , Hydroxyproline/biosynthesis , Interleukin-10/biosynthesis , Interleukin-6/biosynthesis , JNK Mitogen-Activated Protein Kinases/metabolism , Lipid Peroxidation/drug effects , Liver/drug effects , Liver/metabolism , Liver/pathology , Liver Cirrhosis/chemically induced , Liver Cirrhosis/metabolism , Liver Cirrhosis/pathology , Male , Matrix Metalloproteinase 2/biosynthesis , NF-kappa B/biosynthesis , Oxidative Stress/drug effects , RNA, Messenger/genetics , RNA, Messenger/metabolism , Random Allocation , Rats , Rats, Sprague-Dawley , Tissue Inhibitor of Metalloproteinase-1/biosynthesis , Toll-Like Receptor 4/biosynthesis , Transforming Growth Factor beta1/biosynthesis , Tumor Necrosis Factor-alpha/biosynthesis
9.
J Ethnopharmacol ; 136(2): 297-304, 2011 Jun 22.
Article in English | MEDLINE | ID: mdl-21569830

ABSTRACT

AIM OF THE STUDY: GCSB-5 (traditional name: Chungpa-Juhn), an herbal medicine composed of 6 crude herbs (Saposhnikovia divaricata Schiskin, Achyranthis bidentata Blume, Acanthopanax sessiliflorum Seem, Cibotium baromets J. Smith, Glycine max Meriill, and Eucommia ulmoides Oliver), has been widely used in Asia for treatment of neuropathic and inflammatory diseases. This study investigated the protective effect of GCSB-5 against peripheral nerve injury in vitro and in vivo. MATERIALS AND METHODS: After left sciatic nerve transection, rats received oral administration of GCSB-5 (30, 100, 300, and 600 mg/kg), or saline (vehicle), respectively, once daily for 8 weeks. Motor functional recovery and axonal nerve regeneration were evaluated by measurement of sciatic functional index (SFI), sensory regeneration distance, and gastrocnemius muscle mass ratio. The myelinated axon number was counted by morphometric analysis. In the in vitro study, the effects of GCSB-5 on H(2)O(2)-induced oxidative damage in SH-SY5Y cells were investigated by measurement of cell viability, production of reactive oxygen species (ROS), lipid peroxidation, release of lactate dehydrogenease (LDH), and cellular glutathione contents. Neurite outgrowth was also determined. RESULTS: After 8 weeks of nerve transection, SFI, regeneration distance, and gastrocnemius muscle mass ratio and myelinated axon number showed a significant decrease and these decreases were attenuated by GCSB-5. GCSB-5 significantly inhibited H(2)O(2)-induced cell death and oxidative stress, as evidenced by decreases in production of ROS and lipid peroxidation and release of LDH, and by increase in total GSH content. CONCLUSIONS: The neuroprotective effect afforded by GCSB-5 is due in part to reduced oxidative stress.


Subject(s)
Antioxidants/therapeutic use , Drugs, Chinese Herbal/therapeutic use , Nerve Regeneration/drug effects , Peripheral Nervous System Diseases/drug therapy , Phytotherapy , Sciatic Nerve/drug effects , Trauma, Nervous System/drug therapy , Animals , Antioxidants/metabolism , Antioxidants/pharmacology , Cell Death/drug effects , Drugs, Chinese Herbal/pharmacology , Glutathione/metabolism , L-Lactate Dehydrogenase/metabolism , Male , Motor Activity/drug effects , Muscle, Skeletal/drug effects , Muscle, Skeletal/pathology , Nerve Fibers/drug effects , Nerve Regeneration/physiology , Neuroprotective Agents/pharmacology , Neuroprotective Agents/therapeutic use , Oxidative Stress/drug effects , Peripheral Nervous System Diseases/pathology , Peripheral Nervous System Diseases/physiopathology , Plants, Medicinal , Rats , Rats, Sprague-Dawley , Reactive Oxygen Species/metabolism , Sciatic Nerve/pathology , Sciatic Nerve/physiopathology , Trauma, Nervous System/pathology , Trauma, Nervous System/physiopathology
SELECTION OF CITATIONS
SEARCH DETAIL
...