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Autocrine abscisic acid mediates the UV-B-induced inflammatory response in human granulocytes and keratinocytes.

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UV-B is an abiotic environmental stress in both plants and animals. Abscisic acid (ABA) is a phytohormone regulating fundamental physiological functions in plants, including response to abiotic stress. We previously demonstrated that ABA is an endogenous stress hormone also in animal cells. Here, we

Functional characterization of a synthetic abscisic acid analog with anti-inflammatory activity on human granulocytes and monocytes.

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The phytohormone abscisic acid (ABA), in addition to regulating several important physiological functions in plants, is also produced and released by human granulocytes and monocytes where it stimulates cell activities involved in the innate immune response. Here we describe the properties of an ABA

T cell PPARγ is required for the anti-inflammatory efficacy of abscisic acid against experimental IBD.

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The phytohormone abscisic acid (ABA) has been shown to be effective in ameliorating chronic and acute inflammation. The objective of this study was to investigate whether ABA's anti-inflammatory efficacy in the gut is dependent on peroxisome proliferator-activated receptor γ (PPARγ) in T cells.

Is There A Role for Abscisic Acid, A Proven Anti-Inflammatory Agent, in the Treatment of Ischemic Retinopathies?

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Ischemic retinopathies (IRs) are the main cause of severe visual impairment and sight loss, and are characterized by loss of blood vessels, accompanied by hypoxia, and neovascularization. Actual therapies, based on anti-vascular endothelial growth factor (VEGF) strategies, antioxidants or

Abscisic acid enriched fig extract promotes insulin sensitivity by decreasing systemic inflammation and activating LANCL2 in skeletal muscle

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Abscisic acid is a phytohormone found in fruits and vegetables and is endogenously produced in mammals. In humans and mice, lanthionine synthetase C-like 2 (LANCL2) has been characterized as the natural receptor for ABA. Herein, we characterize the efficacy of a fig fruit extract of ABA in promoting

Dietary abscisic acid ameliorates glucose tolerance and obesity-related inflammation in db/db mice fed high-fat diets.

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OBJECTIVE Despite their efficacy in improving insulin sensitivity, thiazolidinediones (TZDs) are associated with a number of side effects (i.e. weight gain, hepatotoxicity, congestive heart failure) that have limited their use by millions of diabetic patients. We have investigated whether abscisic

Abscisic acid regulates inflammation via ligand-binding domain-independent activation of peroxisome proliferator-activated receptor gamma.

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Abscisic acid (ABA) has shown efficacy in the treatment of diabetes and inflammation; however, its molecular targets and the mechanisms of action underlying its immunomodulatory effects remain unclear. This study investigates the role of peroxisome proliferator-activated receptor γ (PPAR γ) and

Abscisic Acid Supplementation Rescues High Fat Diet-Induced Alterations in Hippocampal Inflammation and IRSs Expression.

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Accumulated evidence indicates that neuroinflammation induces insulin resistance in the brain. Moreover, both processes are intimately linked to neurodegenerative disorders, including Alzheimer's disease. Potential mechanisms underlying insulin resistance include serine phosphorylation of the

Correction to: Abscisic Acid Supplementation Rescues High Fat Diet-Induced Alterations in Hippocampal Inflammation and IRSs Expression.

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The author missed to include the second affiliation of Mariam Atef to the original paper published. With this, the authors published this correction.

Abscisic acid is an endogenous stimulator of insulin release from human pancreatic islets with cyclic ADP ribose as second messenger.

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Abscisic acid (ABA) is a plant stress hormone recently identified as an endogenous pro-inflammatory cytokine in human granulocytes. Because paracrine signaling between pancreatic beta cells and inflammatory cells is increasingly recognized as a pathogenetic mechanism in the metabolic syndrome and

Abscisic Acid Standardized Fig (Ficus carica) Extracts Ameliorate Postprandial Glycemic and Insulinemic Responses in Healthy Adults.

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Abscisic acid (ABA) can improve glucose homeostasis and reduce inflammation in mammals by activating lanthionine synthetase C-like 2 (LANCL2). This study examined the effects of two fig fruit extracts (FFEs), each administered at two different ABA doses, on glycemic index (GI) and insulinemic index

Synthesis, structural characterization and effect on human granulocyte intracellular cAMP levels of abscisic acid analogs.

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The phytohormone abscisic acid (ABA), in addition to regulating physiological functions in plants, is also produced and released by several mammalian cell types, including human granulocytes, where it stimulates innate immune functions via an increase of the intracellular cAMP concentration

Abscisic acid - an anti-angiogenic phytohormone that modulates the phenotypical plasticity of endothelial cells and macrophages.

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Abscisic acid (ABA) has shown anti-inflammatory and immunoregulatory properties in preclinical models of diabetes and inflammation. Herein, we studied the effects of ABA on angiogenesis, a strictly controlled process that, when dysregulated, leads to severe angiogenic disorders including vascular

Phytohormone abscisic acid ameliorates cognitive impairments in streptozotocin-induced rat model of Alzheimer's disease through PPARβ/δ and PKA signaling.

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Aim: Alzheimer's disease (AD) is characterized by oxidative stress, neuroinflammation and progressive cognitive decline. Abscisic acid (ABA) is produced in a variety of mammalian tissues, including brain. It has anti-inflammatory and antioxidant effects and elicits a positive effect on

Expression of PPAR γ in intestinal epithelial cells is dispensable for the prevention of colitis by dietary abscisic acid.

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OBJECTIVE Dietary abscisic acid (ABA) has shown efficacy in ameliorating experimental IBD in mice through mechanisms requiring expression of peroxisome proliferator activated-receptor γ (PPAR γ) in immune cells. The goal of this study was to determine whether PPAR γ expression in colonic epithelial

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