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Dental Disease, Inflammation, Cardiovascular Disease, Nutrition and Nutritional Supplements
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
Douglas G. Thompson, Gregori M. Kurtzman, Chelsea Q. Watkins
Biological resolution of inflammation is driven largely by resolvins, lipoxins, maresins and protectins. Collectively coined specialized pro-resolving mediators (SPMs), these endogenous molecules are oxygenated polyunsaturated fatty acids biosynthesized by enzymes lipoxygenases and cyclooxygenases. These chemically sensitive molecules produced in nano- to pico-gram amounts in vivo exhibit potent anti-inflammatory and pro-resolving bioactions. They help clear bacterial infections, while reducing pain and displaying bioactivities toward host defense, organ protection and tissue remodeling.118 Statins, like aspirin, have demonstrated anti-inflammatory and bone-preserving actions by upregulating production of SPMs. Emerging evidence from novel drugs, including SPMs and complement inhibitors, suggests future availability of adjunctive therapeutic strategies for the management of periodontal disease.119
Macronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Since the human body lacks the enzymes needed to synthesize the polyunsaturated fatty acids (PUFAs), α-linolenic (ALA) and linoleic acids (LA) in the diet are its only source. The rate of conversion of α-linolenic omega-3 fatty acid (ALA) into DHA (docosahexaenoic acid) and eicosapentaenoic acid (EPA) is decelerated because of the decreased activity of the Δ6 desaturase in the human body. That is why only 0.2–2% of the dietary ALA is converted into DHA and EPA, while the rest undergoes β-oxidation (102). Therefore, dietary intake of EPA and DHA from fish and crustaceans is needed. EPA and DHA omega-3 acids are also recognized as precursors for the synthesis of novel specialized pro-resolving mediators (SPMs). SPMs include resolvins, protectins, and maresins. Resolvins are synthesized from both EPA and DHA, while maresins and protectins are synthesized from DHA (95). First, EPA and DHA decrease the production of arachidonic acid-derived eicosanoids; then, SPMs activate the resolution of inflammation (95). Hence, a lack of the omega-3 PUFAs, especially EPA and DHA, may not favor resolution of inflammation and may, in fact, promote the pathogenesis of various diseases in which inflammation is involved. Therefore, increased intake of omega-3 fatty acids may decrease inflammation.
Perioperative Metabolic Therapies in Orthopedics
Published in Kohlstadt Ingrid, Cintron Kenneth, Metabolic Therapies in Orthopedics, Second Edition, 2018
Fish oil-derived omega-3 fatty acids displacing the arachidonic acid of the cell membrane of immune cells attenuate the production of inflammatory prostaglandins and prostacyclins and reduce the cytotoxicity of inflammatory cells.2 The essential fatty acids eicosapentaenoic (EPA) and docosahexaenoic acids (DHAs) are the precursors of resolvins, protectins, and maresins: mediators that aid in the resolution of the inflammatory arachidonic acid cascade and are shown to reduce cellular inflammation by inhibiting the transportation of inflammatory cells and mediators to the site of inflammation.77
Targeting endoplasmic reticulum stress—the responder to lipotoxicity and modulator of non-alcoholic fatty liver diseases
Published in Expert Opinion on Therapeutic Targets, 2022
Yu Luo, Qiangqiang Jiao, Yuping Chen
Owing to the critical role of calcium homeostasis in ER function and the tight association of lipotoxicity-induced ER stress with ER calcium depletion [16,17], the SERCA2b, a Ca2+ ATPase on ER membrane, has been serving as a good therapeutic target for suppressing ER stress and NAFLD. Maresin 1 is a proinflammatory regressive mediator and could successfully alleviate ER stress and hepatosteatosis in HFD mice by upregulating SERCA2b [103]. The amelioration of SFAs-induced lipotoxicity in hepatocytes by oleic acid seemed to be correlated with SERCA too [17]. In fact, SERCA2b-targeted agents have successively achieved a nice suppression of hepatosteatosis in HFD animals. MiR‐30b antimiR suppressed ER stress and insulin resistance by upregulating SERCA2b expression in the liver of HFD–treated rats [18]. In addition, the augmenter of liver regeneration (ALR) that enhances the effects of BCL-2 and IP3R, also inhibited ER calcium loss to mitigate the PA-induced ER stress [19] and effectively improved the MCD-induced steatosis and inflammation in mice [104]. No doubt, precisely blocking calcium leakage from ER would be a potential treatment strategy for lipotoxicity-induced hepatocyte injury.
Emerging molecular therapeutic targets for spinal cord injury
Published in Expert Opinion on Therapeutic Targets, 2019
Shuo Wang, George M Smith, Michael E. Selzer, Shuxin Li
The strategies that suppress M1 macrophage activities and enhance M2 macrophage functions are beneficial for tissue repair and recovery. Because the microenvironment around lesions usually favor M1 activation, transplantation of M2 macrophages into lesioned spinal cord preserves neurons, glia, and myelin and enhances functional recovery in SCI rodents [12]. Because M1 and M2 are activated by different chemicals (e.g., M1 by IFN-γ, LPS and MCP-1 vs. M2 by IL-4 and IL-10), modifying the macrophage milieu by altering the concentrations of these chemicals in the lesion area may facilitate neural repair. Liposomes, vesicles with a lipid bilayer, have been used to deliver certain chemicals for modifying macrophage functions because macrophages engulf liposome-conjugated chemicals and release them intracellularly. Liposomal prednisolone phosphate suppresses the M1 phenotype, promotes the M2 phenotype, and protects injured tissues [13]. Deletion of CD36, the most abundant lipid transporter in macrophages, decreases macrophage lipid content and lesion size and improves locomotor recovery in SCI rodents [14]. Systemic delivery of maresin-1, a pro-resolving lipid mediator, also reduces macrophage accumulation and lesion pathology and promotes functional recovery.
Inflammation resolution and specialized pro-resolving lipid mediators in chronic rhinosinusitis
Published in Expert Review of Clinical Immunology, 2023
Peyton Z. Robinson, Daniel N. Frank, Vijay R. Ramakrishnan
D-series resolvins are derived from DHA by 15-LOX and 5-LOX [41]. Importantly, RvDs elicit phenotypic shifts in macrophages from the M1 to M2, allowing for a more permissive environment for inflammatory resolution [55]. Maresins and protectins are produced similarly to the D-series resolvins, as they are also derived from DHA via LOX enzymes. Maresins are unique in their ability to be produced by macrophages, while also being involved in the transition from the M1 to M2 macrophage phenotype and promoting regeneration of tissue [56]. Protectins have been noted for their neuroprotective activity in which they can limit neuronal injury by reducing NF-kB activity, enhancing phagocytosis, limiting leukocyte migration, and facilitating other pro-resolving functions [57].