Cardiac inflammatory disease represents a significant public health burden, and interesting questions of immunopathologic science and clinical inquiry. Novel insights into the diverse programming and functions within the macrophage lineages in recent years have yielded a view of these cells as dynamic effectors and regulators of immunity, host defense, and inflammatory disease. In this review, we examine and discuss recent investigations into the complex participation of mononuclear phagocytic cells in the pathology of animal models of myocarditis.
"The inflammation that occurs during innate immune responses is largely regulated by macrophages  . This inflammation is driven by immunopathological events such as the overproduction of various proinflammatory cytokines, including tumor necrosis factor (TNF-α), interleukin (IL- 1β), interferon (IFN-β), and several types of inflammatory mediators, including nitric oxide (NO) and prostaglandin E 2 (PGE 2 ) . "
[Show abstract][Hide abstract] ABSTRACT: Inflammation is a complex biological response of tissues to harmful stimuli such as pathogens, cell damage, or irritants. Inflammation is considered to be a major cause of most chronic diseases, especially in more than 100 types of inflammatory diseases which include Alzheimer's disease, rheumatoid arthritis, asthma, atherosclerosis, Crohn's disease, colitis, dermatitis, hepatitis, and Parkinson's disease. Recently, an increasing number of studies have focused on inflammatory diseases. TBK1 is a serine/threonine-protein kinase which regulates antiviral defense, host-virus interaction, and immunity. It is ubiquitously expressed in mouse stomach, colon, thymus, and liver. Interestingly, high levels of active TBK1 have also been found to be associated with inflammatory diseases, indicating that TBK1 is closely related to inflammatory responses. Even though relatively few studies have addressed the functional roles of TBK1 relating to inflammation, this paper discusses some recent findings that support the critical role of TBK1 in inflammatory diseases and underlie the necessity of trials to develop useful remedies or therapeutics that target TBK1 for the treatment of inflammatory diseases.
Mediators of Inflammation 12/2012; 2012:979105. DOI:10.1155/2012/979105 · 3.24 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The purpose of this study was to develop triamcinolone acetonide-loaded polyurethane implants (TA PU implants) for the local treatment of different pathologies including arthritis, ocular and neuroinflammatory disorders. The TA PU implants were characterized by FTIR, SAXS and WAXS. The in vitro and in vivo release of TA from the PU implants was evaluated. The efficacy of TA PU implants in suppressing inflammatory-angiogenesis in a murine sponge model was demonstrated. FTIR results revealed no chemical interactions between polymer and drug. SAXS results indicated that the incorporation of the drug did not disturb the polymer morphology. WAXS showed that the crystalline nature of the TA was preserved after incorporation into the PU. The TA released from the PU implants efficiently inhibited the inflammatory-angiogenesis induced by sponge discs in an experimental animal model. Finally, TA PU implants could be used as local drug delivery systems because of their controlled delivery of TA.
Journal of Materials Science Materials in Medicine 04/2012; 23(6):1431-45. DOI:10.1007/s10856-012-4615-5 · 2.59 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Arbutin, which is found in the genus Arctostaphylos, is an anti-oxidant and a depigmenting agent. The present study was designed to validate the anti-inflammatory effect of arbutin.
The anti-inflammatory properties of arbutin were studied using a lipopolysaccharide (LPS)-stimulated murine BV2 microglial cells model. As inflammatory parameters, the production of nitric oxide (NO), inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), monocyte chemoattractant protein-1 (MCP-1), and interleukin-6 (IL-6) were evaluated. We also examined the expression of ninjurin1 (Ninj1) and the adhesion activity of BV2 cells. Finally, we analyzed the activation of the nuclear factor-κB (NF-κB) signaling pathway.
Arbutin suppressed LPS-induced production of NO and expression of iNOS and COX-2 in a dose-dependent manner without causing cellular toxicity. Arbutin also significantly reduced generation of proinflammatory cytokines, including IL-1β and TNF-α, and other inflammation-related genes such as MCP-1 and IL-6. Additionally, arbutin suppressed the adhesion activity of BV2 cells and the expression of an important adhesion molecule, Ninj1, in LPS-stimulated murine BV2 cells. Furthermore, arbutin inhibited nuclear translocation and the transcriptional activity of NF-κB.
Taken together, our results suggest that arbutin might be useful for treating the inflammatory and deleterious effects of BV2 microglial cells activation in response to LPS stimulation.
Agents and Actions 04/2012; 61(8):817-25. DOI:10.1007/s00011-012-0474-2 · 2.35 Impact Factor
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