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Sivu 1 alkaen 1652 tuloksia
Modulating inflammation in a cutaneous chronic wound model by IL-10 released from collagen-silica nanocomposites via gene delivery.
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Cutaneous chronic wounds remain a major clinical challenge which requires the development of novel wound dressings. Previously, we showed that collagen-silica nanocomposites consisting of polyethyleneimine (PEI)-DNA complexes associated with silica nanoparticles (SiNP), collagen hydrogel and 3T3
Comparison of low doses of aged and freshly fractured silica on pulmonary inflammation and damage in the rat.
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Most previous studies of silica toxicity have used relatively high exposure doses of silica. In this study, male rats received by intratracheal instillation either vehicle, aged or freshly fractured silica at a dose of either 5 microg/rat once a week for 12 weeks (total dose=60 microg) or 20
Acute NO2 exposure alters inflammatory cell activation and particle clearance in silica-injected mice.
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Previous work indicates that exposure to nitrogen dioxide (NO2) at different stages of silica-induced acute inflammation alters the outcome of lung injury. C57BI/6 mice were injected intratracheally (IT) with 2.0 mg silica particles (SI) and subsequently exposed to 20 ppm NO2 (or filtered air)
Subchronic pulmonary inflammation and fibrosis induced by silica in rats are attenuated by amiodarone.
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A previous study demonstrated that the acute phase of silica-induced lung injury in rats can be attenuated by concomitant administration of amiodarone, a cationic amphiphilic drug that inhibits phospholipase activity in the lungs. The purpose of the present study was to determine whether continued
The alarmin IL-1α is a master cytokine in acute lung inflammation induced by silica micro- and nanoparticles.
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BACKGROUND
Inflammasome-activated IL-1β plays a major role in lung neutrophilic inflammation induced by inhaled silica. However, the exact mechanisms that contribute to the initial production of precursor IL-1β (pro-IL-1β) are still unclear. Here, we assessed the implication of alarmins (IL-1α,
Blocking the 4-1BB Pathway Ameliorates Crystalline Silica-induced Lung Inflammation and Fibrosis in Mice.
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Long term pulmonary exposure to crystalline silica leads to silicosis that manifests progressive interstitial fibrosis, eventually leading to respiratory failure and death. Despite efforts to eliminate silicosis, clinical cases continue to occur in both developing and developed countries. The exact
Comparative RNA-Seq transcriptome analysis on silica induced pulmonary inflammation and fibrosis in mice silicosis model.
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Silicosis is a long-established public health issue in developing countries due to increasingly serious air pollution and poorly implemented occupational safety regulation. Inhalation of silica triggers cytotoxicity, oxidative stress, pulmonary inflammation and eventually silicosis. Current
Incorporation of anti-inflammatory agent into mesoporous silica.
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The unique properties of macroporous, mesoporous, and microporous systems, including their ability to accommodate molecules of different sizes inside their pores and to act as drug delivery systems, have been the object of extensive studies. In this work, mesoporous silica with hexagonal structure
In vitro Dissolution, Cellular Membrane Permeability and Anti-Inflammatory Response of Resveratrol-Encapsulated Mesoporous Silica Nanoparticles.
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Sizing drugs down to the submicron and nanometer scale using nanoparticles has been extensively used in pharmaceutical industries to overcome the poor aqueous solubility of potential therapeutic agents. Here, we report the encapsulation and release of resveratrol, a promising anti-inflammatory and
ATM-activated autotaxin (ATX) propagates inflammation and DNA damage in lung epithelial cells; a new mode of action for silica-induced DNA damage?
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Silica exposure is a common risk factor for lung cancer. It has been claimed that key elements in cancer development are activation of inflammatory cells that indirectly induce DNA damage and proliferative stimuli in respiratory epithelial cells. We studied DNA damage induced by silica particles in
Complement facilitates macrophage phagocytosis of inhaled iron particles but has little effect in mediating silica-induced lung inflammatory and clearance responses.
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Complement-mediated mechanisms are known to play a role in pulmonary inflammation and clearance responses to some types of inhaled particles. The present studies were undertaken to investigate the role of complement in mediating pulmonary inflammation and/or phagocytosis as a function of particle
Silica-induced pulmonary inflammation and fibrosis in mice is altered by acute exposure to nitrogen dioxide.
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The biologic impact of consecutive exposures to two environmental pollutants was examined in mice exposed to silica crystals (SI) by intratracheal (IT) injection followed by an inhalation exposure to nitrogen dioxide (NO2). C57Bl/6 mice received an IT injection of 2 mg SI or sterile saline (SAL)
Amorphous silica nanoparticles impair vascular homeostasis and induce systemic inflammation.
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Amorphous silica nanoparticles (SiNPs) are being used in biomedical, pharmaceutical, and many other industrial applications entailing human exposure. However, their potential vascular and systemic pathophysiologic effects are not fully understood. Here, we investigated the acute (24 hours) systemic
Exogenous Gas6 attenuates silica-induced inflammation on differentiated THP-1 macrophages.
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Growth arrest specific 6 (Gas6) has been reported to be related to the modulation of innate immunity. To investigate the potential effect of Gas6 on the regulation of inflammations induced by silica, differentiated THP-1 macrophages were exposed to different concentrations of silica for 6h and 24h.
Silica and double-stranded RNA synergistically induce bronchial epithelial apoptosis and airway inflammation.
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Silica crystals (silica), which are the main mineral component of volcanic ash and desert dust, can activate the caspase-1-activating inflammasome in phagocytic cells to secrete IL-1β. Although inhalation of silica-containing dust is known to exacerbate chronic respiratory diseases, probably through
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