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244 results for “lipopolysaccharide”
Fig. 6 in Glycoglycerolipids from the leaves of Perilla frutescens (L.) Britton (Labiatae) and their anti-inflammatory activities in lipopolysaccharide-stimulated RAW264.7 cells
Fig. 6. Inhibitory effects of three glycoglycerolipids on pro-inflammatory cytokines (IL-6, TNF-α, and IL-1β) secretion in 200 ng/ml LPS-stimulated murine macrophages RAW 264.7 cells after 24 h incubation. Different lowercase letters above the bars represented the significant difference (P <0.05) (+: presence; -: absence).
Fig. 5 in Glycoglycerolipids from the leaves of Perilla frutescens (L.) Britton (Labiatae) and their anti-inflammatory activities in lipopolysaccharide-stimulated RAW264.7 cells
Fig. 5. Inhibitory effects of three glycoglycerolipids from Perilla frutescens leaves on the production of NO in 200 ng/ml LPS-stimulated murine macrophages RAW 264.7 cells. Different lowercase letters above the bars represented the significant difference (P <0.05) (+: presence; -: absence).
Fig. 3. 2D in Glycoglycerolipids from the leaves of Perilla frutescens (L.) Britton (Labiatae) and their anti-inflammatory activities in lipopolysaccharide-stimulated RAW264.7 cells
Fig. 3. 2D NMR spectra of compounds 1, 2 and 3 and structure of compounds 1. (A) Partial HMQC NMR spectrum of compound 1 (CDCl3, 600 MHz), see Supplementary Figs. 6 for the complete HMQC NMR spectrum of compound 1; (B) TCOSY NMR spectrum of compound 1 (CDCl3, 600 MHz); (C) HMBC NMR spectrum of compound 1 (CDCl, 600 MHz); (D) Structure of compound 1. (E) Key 1H–1H TCOSY (─) and HMBC (→) correlations in compound 2. (F) Key 1H–1H TCOSY (─) and 3 HMBC (→) correlations in compound 3.
Fig. 2 in Glycoglycerolipids from the leaves of Perilla frutescens (L.) Britton (Labiatae) and their anti-inflammatory activities in lipopolysaccharide-stimulated RAW264.7 cells
Fig. 2. Positive-ion MALDI-TOF/TOF-MS/MS spectrum of MGDG and DGDG from Perilla frutescens leaves. (A) Compound 1 (MGDG); (B) Compound 2 (DGDG); and (C) Compound 3 (DGDG).
Effects of ferulic acid on growth performance and intestinal oxidation indexes of Jilin white geese under lipopolysaccharide-induced oxidative stress
<p>In geese breeding, due to the frequent influence of drugs and environmental and other factors, geese are extremely prone to oxidative stress, which adversely affects growth and development, geese meat quality, down production, and severely affects the development of the geese industry. Ferulic acid from plant extracts can be used as a feed additive, which is safe and non-toxic, and it can exert certain therapeutic effects on oxidative stress in geese. This experiment investigated the effect of ferulic acid on the growth performance, organs indices, and intestinal oxidative indices of Jilin white geese under lipopolysaccharide-induced oxidative stress. Geese were randomly divided into six groups: C (blank control), L (lipopolysaccharide control), F1 (60 mg/kg ferulic acid), F2 (120 mg/kg ferulic acid), F3 (180 mg/kg ferulic acid), and F4 (240 mg/kg ferulic acid). Groups L and F1–F4 were injected intraperitoneally with 0.5 mg/kg lipopolysaccharide and group C with an equivalent volume of normal saline on days 14,17 and 20, and 10 animals from each group were randomly selected for slaughter on day 21. The results showed that: 1) On day 14, the final body weight and average daily feed intake were significantly higher in group F3 than in group L, and on day 21, the final body weight was significantly higher in group F3 than in group L. 2) The thymus index was significantly higher in group F4 than in group L. 4) In the duodenum, MDA activity was reduced in group C compared with that in group L. 5) In the jejunum and ileum, MDA was significantly lower in group F3 than in group L. These results show that the addition of 180 mg/kg of ferulic acid to the diet can promote the growth of geese and alleviate the damage caused by oxidative stress in all intestinal segments.</p>
Increased Gut Permeability to Lipopolysaccharides (LPS) in Parkinson's Disease
ClinicalTrials.gov study NCT01155492. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Neutrophil Imaging in Healthy Subjects Following Lipopolysaccharide or Saline Challenge and in Subjects With Chronic Obstructive Pulmonary Disease
ClinicalTrials.gov study NCT02551614. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Lipopolysaccharide Adsorption At Septic Shock
ClinicalTrials.gov study NCT04827407. IPD Sharing: NO. Countries: 1. Publications: 1.
Lipoprotein Metabolism and Bacterial Lipopolysaccharide in Parkinson's Disease
ClinicalTrials.gov study NCT03937284. IPD Sharing: Not stated. Countries: 1. Publications: 5.
Link Between Plasma Citrulline and Lipopolysaccharide Concentrations in the Critically Ill
ClinicalTrials.gov study NCT02902276. IPD Sharing: NO. Countries: 1. Publications: 1.
Effect of Intrapulmonary Recombinant Human Activated Protein C (APC) on Coagulation and Inflammation After Lipopolysaccharide (LPS)
ClinicalTrials.gov study NCT00943267. IPD Sharing: Not stated. Countries: 1. Publications: 1.
A Methodology Study in Healthy Subjects to Evaluate the Effect of AZD8309 After Nasal Administration of Lipopolysaccharide (LPS)
ClinicalTrials.gov study NCT00860821. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Effect of Antioxidants on Oxygen Induced Vasoconstriction in Lipopolysaccharide (LPS) Induced Inflammatory Model in Humans
ClinicalTrials.gov study NCT00914576. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Development of Novel Non-invasive Inflammometry Following Lipopolysaccharide, Endotoxin (LPS) Challenge in Healthy Volunteers
ClinicalTrials.gov study NCT03044327. IPD Sharing: NO. Countries: 1. Publications: 2.
Suitability of a Low Dose Lipopolysaccharide (LPS) Inhalation as a Challenge Model
ClinicalTrials.gov study NCT01400568. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Clinical Relevance of the Reverse Lipopolysaccharide Transport Pathway in Patients With Acute Peritonitis
ClinicalTrials.gov study NCT04126577. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Movement of Arginine Through OprD: The Energetics of Permeation and The Role of Lipopolysaccharide in Directing Arginine to The Protein
<p>The outer membrane channel OprD from <em>Pseudomonas aeruginosa</em> transports basic amino acids and clinically relevant carbapenem antibiotics. Understanding the molecular basis of substrate permeation across this channel will therefore lead to better therapeutic designs to treat infections. Using umbrella sampling simulations, we calculated the potential of mean force (PMF) for the arginine permeation pathway through OprD. The PMF reveals a deep free energy well of ∼6 <em>kT</em>around the putative substrate binding site followed by a shallower well of ∼4 <em>kT</em> close to the most constricted region of the pore. Despite becoming partially dehydrated during translocation, some water molecules are retained to shield the guanidinium side chain of arginine from the ladder of basic residues in the protein. Sugars of the lipopolysaccharide headgroups form contacts with arginine and could potentially play an important role in transferring substrate from the external medium to OprD. The PMF through bulk membrane shows a large energetic barrier of ∼45 <em>kT</em> within the hydrophobic core of the membrane, suggesting that spontaneous translocation without OprD is highly unlikely. This significant energetic penalty is likely caused by the extensive distortion of the lower leaflet of the outer membrane as phospholipid headgroups sink inwards to interact with charged groups of arginine. Our results provide quantitative insights into solute permeation across the bacterial outer membrane.</p>
Supplemental materials for Glucocorticoid production in lymphoid organs: Acute effects of lipopolysaccharide in neonatal and adult mice
<p>Supplemental materials for "Glucocorticoid production in lymphoid organs: Acute effects of lipopolysaccharide in neonatal and adult mice" submitted to <em>Endocrinology</em>.</p> <p><strong>Abstract:</strong><br> Glucocorticoids (GCs) are critical modulators of the immune system. The hypothalamic-pituitary-adrenal (HPA) axis regulates circulating GC levels and is stimulated by endotoxins. Lymphoid organs also produce GCs; however, it is not known how lymphoid GC levels are regulated in response to endotoxins. We assessed whether an acute challenge of lipopolysaccharide (LPS) increases lymphoid levels of GCs, steroidogenic enzymes expression, and components of the HPA axis (e.g., CRH) expression. We administered LPS (50µg/kg i.p.) or vehicle control to male and female C57BL/6J neonatal (post-natal day (PND) 5) and adult (PND90) mice and collected blood, bone marrow, thymus, and spleen 4 hr later. We measured progesterone, 11-deoxycorticosterone (DOC), corticosterone, and 11-dehydrocorticosterone (DHC) via liquid chromatography tandem mass spectrometry (LC-MS/MS). We measured gene expression of key steroidogenic enzymes (<em>Cyp11b1</em>, <em>Hsd11b1</em>, and <em>Hsd11b2</em>) and HPA axis components (<em>Crh</em>, <em>Crhr1</em>, <em>Pomc</em>, and <em>Mc2r</em>) via qPCR. At PND5, LPS induced greater increases in steroid levels in lymphoid organs than in blood. In contrast, at PND90, LPS induced greater increases in steroid levels in blood than in lymphoid organs. Steroidogenic enzyme transcripts were present in all lymphoid organs, and LPS altered steroidogenic enzyme expression predominately in the spleen. Lastly, we detected transcripts of key HPA axis components in all lymphoid organs, and there was an effect of LPS in the spleen. Taken together, these data suggest that LPS regulates GC production by lymphoid organs, similar to its effects on the adrenal glands, and the effects of LPS might be mediated by local expression of CRH and ACTH.</p>
Figure 9 in All aspects of the toxic effects of lipopolysaccharide on rat liver and the protective effect of vitamin E and sodium selenite
Figure 9. LPS group with VE and SS in male rat liver, showing PCNA protein expression with immunohistochemical analysis. (a, b) LPS, (c) LPS + VE, (d) LPS + SS, and (e, f) LPS + SS + VE groups. Single arrow PCNA expression in the LPS, LPS and/or VE + SS groups show multiple apoptotic cells at 200×.
Figure 5 in All aspects of the toxic effects of lipopolysaccharide on rat liver and the protective effect of vitamin E and sodium selenite
Figure 5. Liver sections of LPS + VE-treated rats. (A) Showing ⇑: dilation of the sinusoids, *: necrosis, and ►: vacuolar degeneration; and (B) ↑↑: vascular congestion and ⇒: hemorrhage at 200×.
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Allen Brain Atlas
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Annotated Behaviour and Observability Dataset (ABODe)
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