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Controlled Delivery Models of Bioactive Factors for the Maturation of Engineered Tissues
Published in Emmanuel Opara, Controlled Drug Delivery Systems, 2020
Ashkan Shafiee, Elham Ghadiri, Jareer Kassis, Anthony Atala
Sustained localized delivery of FTY720 was accomplished using a continuous polymer coating system. The FTY720 was encapsulated with polylactic-co-glycolic acid, which in turn was coated onto the devitalized bone allograft. This system showed a 64% delivery efficacy over a period of 14 days. Separately, prostaglandin E2 has been found to be helpful for cardiovascular tissue regeneration66 and bone regeneration. A drug delivery system using a cholesterol-bearing pullulan nanogel suspended in saline was fabricated to deliver prostaglandin E2 locally.67 The prostaglandin E2 was also dissolved in saline, ethanol, and Tween-80, and was delivered as this composite.
Polymers
Published in Bryan Ellis, Ray Smith, Polymers, 2008
Miscellaneous: Constit. of leaf juice of Aloe barbadensis and Aloe arborescens (Liliaceae). Biol. active component of carrisyn extract (73-90%). Potent inducer of Interleukin 1 and Prostaglandin E2 production by human peripheral blood adherent cells in vitro. Influences activity and production of T-lymphocytes, fibroblasts, B-lymphocytes and endothelial cells. Adjuvant and immunoen- hancer. Increases antibody production, stimulates phagocytosis. Shows specific antineoplastic activity against sarcoid tumours in horse. Used in the treatment of inflammatory bowel disease
Terpenoids in Treatment of Immunological Disease
Published in Dijendra Nath Roy, Terpenoids Against Human Diseases, 2019
Avik Sarkar, Surajit Bhattacharjee
Generation of inflammatory responses in the host is dependent on both innate and adaptive immune responses. Various cells like dendritic cells, macrophages, natural killer cells and mast cells are involved in the innate immune response against inflammatory disorders, whereas, more specialized cells like B lymphocytes and T lymphocytes are responsible for the adaptive immune responses. Inflammatory responses are regulated by numerous mediators that are usually divided into two main classes as pro-inflammatory and anti-inflammatory. Host molecules like eicosanoids, cytokines and chemokines are the principal inflammatory mediators involved in the pathogenesis associated with inflammation (Turner et al., 2014). Tumour necrosis factor-alpha (TNF-α), interferon (IFN)-γ, interleukin-12 (IL-12) and IL-1α are important cytokines which exert pro-inflammatory response in multiple immune diseases. IL-1α has also been reported to exhibit anti-inflammatory activity (Schuerwegh et al., 2003). Other important cytokines include IL-6, IL-8, IL-23, IL-27 and IL-35, which are known for their inflammatory responses against various pathological conditions (Arican et al., 2005; Bobryshev et al., 2015; Casella et al., 2017). IL-10, however, is an anti-inflammatory cytokine which interferes with the functionalities of pro-inflammatory cytokines and helps maintain homeostasis (Couper et al., 2010). Amongst the eicosanoids, prostaglandin E2 (PGE2) is reported to be associated with pathological conditions resulted from heightened inflammatory responses. Phospholipase A2 (PLA2) and the cyclooxygenases (COX) are the principal enzymes involved in the formation of prostaglandins from arachidonic acid. Therefore, any abnormalities in these two groups of enzymes result in inflammatory diseases. Leukotrienes (LTs) are another group of eicosanoids involved in the inflammatory response and linked to diseases like asthma and other autoimmune disorders (O’Byrne 1997; Simopoulos 2002). Enzymes like 5-lipooxygenase (5-LOX) play a determinant role in the synthesis of LTs and are associated with the inflammatory response (Wisastra and Dekker 2014). Another enzyme that is highly associated with inflammatory conditions is nitric oxide synthase (NOS), which catalyses nitric oxide (NO) synthesis from the oxidation of the amino acid l-arginine. Like COX-2, inducible NOS (iNOS) has been reported to be one of the most crucial pro-inflammatory NOS isoforms (Soufli et al., 2016). Nuclear factor-kappa B (NF-κB) is one of the major transcription factors and is associated with regulating expression of signalling molecules that are responsible for immune and inflammatory responses (Lawrence 2009). Activation of this molecule takes place by nuclear transportation of its cytoplasmic complex, causing transcription of pro-inflammatory genes. In mammals, the NF-κB machinery comprise several members (NF-κB1 [p50/p105], NF-κB2 [p52/p100], p65 [RelA], RelB and c-Rel) which act as transactivation domains necessary for gene regulation in physiological and pathological processes associated with inflammation (Oeckinghaus and Ghosh 2009).
Effect of phosphodiester composition in polyphosphoesters on the inhibition of osteoclastic differentiation of murine bone marrow mononuclear cells
Published in Journal of Biomaterials Science, Polymer Edition, 2023
Sota Fukaura, Yasuhiko Iwasaki
1,5,7-Triazabicyclo[4.4.0]dec-5-ene (TBD) was purchased from Sigma-Aldrich Co. (St. Louis, MO, USA) and used without purification. TRAP staining kit was purchased from Sigma-Aldrich Co. (St. Louis, MO, USA) and used following the manufacturer’s protocol. Cytoskeleton Inc. (Denver, CO, USA) supplied fluorescence-labeled phalloidin (Acti-StainTM 535). Recombinant macrophage colony-stimulating factor (M-CSF) and recombinant receptor activator of nuclear factor-kB ligand (RANKL) were purchased from PeproTech, Inc. (Rocky Hill, NJ, USA). Prostaglandin E2 (PGE2) was obtained from Cayman Chemical (Ann Arbor, MI, USA). Real-time PCR reagents and primers were obtained from Takara Bio (Otsu, Japan) and Life Technologies Japan Ltd. (Tokyo, Japan). Table S1 lists the primers used in this study. Other chemicals were purchased from Fujifilm Wako Pure Chemical Co. (Osaka, Japan) as extra-pure grades and were used without further purification. Water was purified using a Merk Millipore Simplicity UV system, which involves UV irradiation, ion exchange, activated carbon adsorption, and filtration (18.2 MΩ cm).
Anti-inflammatory mechanisms of fruits and by-products from Mauritia flexuosa, an exotic plant with functional benefits#
Published in Journal of Toxicology and Environmental Health, Part A, 2021
Vivianne Rodrigues Amorim, Débora Caroline do Nascimento Rodrigues, Jurandy do Nascimento Silva, Carla Lorena Silva Ramos, Lívia Maria Nunes Almeida, Antonia Amanda Cardoso Almeida, Flaviano Ribeiro Pinheiro-Neto, Fernanda Regina Castro Almeida, Marcia Santos Rizzo, Joilane Alves Pereira-Freire, Paulo Michel Pinheiro Ferreira
Carrageenan, a sulfated polysaccharide extracted from red algae (Winter, Risley, and Nuss 1962), triggers an acute, nonimmune and highly reproducible inflammatory process, where edema is established for 4 hr and may last up to 96 hr characterized by an exacerbated response to thermal and mechanical stimuli. When injected subcutaneously into the animal intraplantar region, carrageenan induces the classic signs of inflammation including redness, swelling, heat, and pain due to the presence of pro-inflammatory mediators and cells (Barth et al. 2016; Chakrabarty, Mccarson, and Smith 2011). However, regarding mechanistic effects, inflammatory swelling induced by carrageenan is not considered a specific model for assessing anti-inflammatory promising substances because it triggers the release of numerous chemical mediators (Winter, Risley, and Nuss 1962), including those released in the initial phase (0–1 h), as histamine, serotonin and kinins (mainly bradykinin), whose release increases vascular permeability for the posterior phase (1–6 hr), when marked activation of cyclooxygenase-2 initiates higher production of prostaglandins and nitric oxide and infiltration of neutrophils (Chen et al. 2017; Damasceno et al. 2014; Loet al. 1982). Thus, to examine the mechanism(s) of action, additional investigations were conducted using the compound 48/80, serotonin, histamine, and prostaglandin E2.
Mechanisms underlying the healing potentials of the methanol extract of Chasmanthera dependens stem on indomethacin-induced gastric ulcer
Published in Egyptian Journal of Basic and Applied Sciences, 2021
Abiola Stephanie Tijani, Ebenezer Olatunde Farombi, Samuel Babafemi Olaleye
Gastric ulcer is one of the leading chronic ailments of the gastrointestinal tract [1,2] caused by administration of nonsteroidal anti-inflammatory drugs (NSAIDs), alcohol consumption, stress, Helicobacter pylori, smoking and nutritional deficiencies [3]. Untreated gastric ulcers may gradually deteriorate and result in unexpected complications, such as bleeding or perforation [4,5]. Indomethacin is a non-steroidal anti-inflammatory drug with antipyretic, antithrombotic and analgesic effects [6]. Its most common side effect is a gastrointestinal injury like gastric ulcers [7]. Mechanisms involved in indomethacin-induced gastric ulcer include inhibition of cyclooxygenase (COX), an enzyme responsible for prostaglandins synthesis, generation of free radicals, neutrophil infiltration, inhibition of angiogenesis and induction of apoptosis [8–12]. Prostaglandins are cytoprotective agents in the gastric mucosa, they stimulate the secretion of bicarbonate and mucus, maintain mucosal blood flow, and regulate mucosal cell turnover and repair [13]. Inhibition of prostaglandins synthesis, especially prostaglandin E2 (PGE2) by indomethacin and other members of the NSAIDs can slow down the healing process of gastric ulcers through their anti‑inflammatory activity [14].