scholarly journals Peroxisomal Acyl-CoA Oxidase Type 1: Anti-Inflammatory and Anti-Aging Properties with a Special Emphasis on Studies with LPS and Argan Oil as a Model Transposable to Aging

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Joseph Vamecq ◽  
Pierre Andreoletti ◽  
Riad El Kebbaj ◽  
Fatima-Ezzahra Saih ◽  
Norbert Latruffe ◽  
...  
Keyword(s):  
Neurodegenerative Disorders ◽  
Physiological Role ◽  
Nordihydroguaiaretic Acid ◽  
Health And Wellness ◽  
Argan Oil ◽  
Aging Properties ◽  
Acyl Coa Oxidase ◽  
Anti Inflammatory

To clarify appropriateness of current claims for health and wellness virtues of argan oil, studies were conducted in inflammatory states. LPS induces inflammation with reduction of PGC1-α signaling and energy metabolism. Argan oil protected the liver against LPS toxicity and interestingly enough preservation of peroxisomal acyl-CoA oxidase type 1 (ACOX1) activity against depression by LPS. This model of LPS-driven toxicity circumvented by argan oil along with a key anti-inflammatory role attributed to ACOX1 has been here transposed to model aging. This view is consistent with known physiological role of ACOX1 in yielding precursors of specialized proresolving mediators (SPM) and with characteristics of aging and related disorders including reduced PGC1-α function and improvement by strategies rising ACOX1 (via hormonal gut FGF19 and nordihydroguaiaretic acid in metabolic syndrome and diabetes conditions) and SPM (neurodegenerative disorders, atherosclerosis, and stroke). Delay of aging to resolve inflammation results from altered production of SPM, SPM improving most aging disorders. The strategic metabolic place of ACOX1, upstream of SPM biosynthesis, along with ability of ACOX1 preservation/induction and SPM to improve aging-related disorders and known association of aging with drop in ACOX1 and SPM, all converge to conclude that ACOX1 represents a previously unsuspected and currently emerging antiaging protein.

scholarly journals Possible Role of TGF – B Pathways in Schizophrenia / Moguća Uloga TTGF - B Signalnih Puteva U Shizofreniji

2016 ◽  
Vol 17 (1) ◽  
pp. 3-8 ◽  
Author(s):  
Milica Borovcanin ◽  
Ivan Jovanovic ◽  
Slavica Djukic Dejanovic ◽  
Gordana Radosavljevic ◽  
Nebojsa Arsenijevic ◽  
...  
Keyword(s):  
Meta Analysis ◽  
Psychotic Episode ◽  
T Helper ◽  
Helper Cell Type ◽  
State Marker ◽  
Valuable Marker ◽  
Anti Inflammatory

AbstractThe phenomenological uniqueness of each patient with schizophrenia is determined by complex symptomatology, particularly the overlapping of symptoms and their prominence in certain phases of this mental disorder. Establishing biological markers is an important step in the further objectivisation and quantification of schizophrenia. Identifying the cytokine profiles that precede a psychotic episode could direct the strategies for relapse prevention and be useful in predicting disease progression and treatment response. In the context of infl ammation, TGF-β exerts potent anti-inflammatory and immunosuppressive functions by inhibiting pro-inflammatory cytokine synthesis, but it can also have pro-inflammatory functions through its stimulatory effects on inflammatory Th17 cells. It has been shown that the T helper cell type-1 and type-17 responses are reduced and type-2 response is increased in patients with schizophrenia. Both data from the literature and our results also indicate the presence of an anti-inflammatory response through production of the TGF-β regulatory cytokine. A meta-analysis of plasma cytokine alterations suggested that TGF-β is the state marker for acute exacerbation of schizophrenia, and we showed that TGF-β can also be a valuable marker for psychosis. Hyperactivity of TGF-β signalling pathways in schizophrenia may be both a neuroprotective mechanism and a possible therapeutic target.

scholarly journals Update on the Role of Cannabinoid Receptors after Ischemic Stroke

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Luciano S. A. Capettini ◽  
Silvia Q. Savergnini ◽  
Rafaela F. da Silva ◽  
Nikos Stergiopulos ◽  
Robson A. S. Santos ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cannabinoid Receptors ◽  
Inflammatory Diseases ◽  
Receptor Activation ◽  
Protective Effects ◽  
Peripheral Tissues ◽  
Transmembrane Receptors ◽  
Anti Inflammatory

Cannabinoids are considered as key mediators in the pathophysiology of inflammatory diseases, including atherosclerosis. In particular, they have been shown to reduce the ischemic injury after acute cardiovascular events, such as acute myocardial infarction and ischemic stroke. These protective and anti-inflammatory properties on peripheral tissues and circulating inflammatory have been demonstrated to involve their binding with both selective cannabinoid type 1 (CB1) and type 2 (CB2) transmembrane receptors. On the other hands, the recent discoveries of novel different classes of cannabinoids and receptors have increased the complexity of this system in atherosclerosis. Although only preliminary data have been reported on the activities of novel cannabinoid receptors, several studies have already investigated the role ofCB1andCB2receptors in ischemic stroke. WhileCB1receptor activation has been shown to directly reduce atherosclerotic plaque inflammation, controversial data have been shown on neurotransmission and neuroprotection after stroke. Given its potent anti-inflammatory activities on circulating leukocytes, theCB2activation has been proven to produce protective effects against acute poststroke inflammation. In this paper, we will update evidence on different cannabinoid-triggered avenues to reduce inflammation and neuronal injury in acute ischemic stroke.

scholarly journals Proinsulin C-peptide - A Consensus Statement

2001 ◽  
Vol 2 (2) ◽  
pp. 145-151 ◽  
Author(s):  
Anders A. F. Sima ◽  
George Grunberger ◽  
Hans Jörnvall ◽  
John Wahren ◽  
The C-Peptide Study Group
Keyword(s):  
Physiological Role ◽  
Biological Action ◽  
Clinical Effects ◽  
State University ◽  
C Peptide ◽  
Wayne State University ◽  
Therapeutic Value ◽  
Diabetes Center

In recent years the physiological role of the proinsulin C-peptide has received increasing attention, focusing on the potential therapeutic value of C-peptide replacement in preventing and ameliorating type 1 diabetic complications. In order to consolidate these new data and to identify the immediate directions of C-peptide research and its clinical usefulness, an International Symposium was held in Detroit, Michigan, on October 20–21, 2000, under the auspices of the Wayne State University/Morris Hood Jr. Comprehensive Diabetes Center. In this communication, we review the cellular, physiological and clinical effects of C-peptide replacement in animal models and in patients with type 1 diabetes. Finally, recommendations are presented as to the most urgent studies that should be pursued to further establish the biological action of C-peptide and its therapeutic value.

Abstract 590: Loss of Myeloid Cell Prostaglandin E Receptor 4 Does Not Alter Diabetes-Accelerated Atherosclerosis in a Murine Model of Type 1 Diabetes

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Sara N Vallerie ◽  
Farah Kramer ◽  
Jenny E Kanter ◽  
Shelley Barnhart ◽  
Richard M Breyer ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Mouse Model ◽  
Myeloid Cells ◽  
Myeloid Cell ◽  
Prostaglandin E ◽  
Lesion Area ◽  
Accelerated Atherosclerosis ◽  
Anti Inflammatory

Diabetes is associated with an increased risk of cardiovascular disease, largely due to increased atherosclerosis. Our studies have suggested myeloid cell prostaglandin E 2 (PGE 2 ) production as a possible mediator of diabetes-accelerated atherosclerosis in a virally-induced mouse model of type 1 diabetes. Prostaglandin E Receptor 4 (EP4; Ptger4 ) is a major PGE 2 receptor in myeloid cells. We hypothesized that generation of a mouse model of myeloid cell-targeted EP4-deficiency would allow us to test the role of myeloid EP4 in diabetes-accelerated atherosclerosis. Thus, we generated a Ptger4 flox/flox LysM-Cre tg/tg mouse model. Peritoneal macrophages isolated from these myeloid cell EP4-deficient (EP4 M-/- ) mice expressed <90% Ptger4 mRNA compared to LysM-Cre tg/tg controls (n=10; p<0.0001). To analyze the role of myeloid cell EP4 in diabetes-accelerated atherosclerosis, we transplanted bone marrow from EP4 M-/- mice and littermate controls into lethally irradiated Ldlr -/- RIP-LCMV mice (the model of type 1 diabetes) and, after 7 weeks of recovery, induced diabetes by viral infection and fed the mice a low-fat semi-purified diet for an additional 12 weeks. Diabetic EP4 M-/- mice had similar blood glucose (568 ± 15 vs. 569 ± 15 mg/dl), blood cholesterol (531 ± 29 vs. 510 ± 37 mg/dl), and plasma triglycerides (249 ± 49 vs. 247 ± 44 mg/dl) as diabetic controls (n=15 all groups; mean ± SEM). At the endpoint, aortas were harvested for lesion area quantification. Diabetic EP4 M-/- and diabetic wild type mice had similar lesion area (1.9% ± 0.2 vs. 1.7% ± 0.2), which were both increased (p < 0.01; n=9-15) as compared to their non-diabetic controls. Additionally, we analyzed the role of EP4 in inflammatory activation of myeloid cells ex vivo. EP4-deficiency had no significant effect on basal or lipopolysaccharide (LPS)-induced inflammatory gene expression in the absence of PGE 2 . Pretreatment of the cells with PGE 2 (10 nM) followed by LPS stimulation resulted in a significant reduction of Tnfa and Il6 mRNA compared to LPS alone, and this anti-inflammatory effect of PGE 2 was completely blocked in EP4-deficient cells. These results suggest that myeloid cell EP4 mediates anti-inflammatory actions of PGE 2 but that it is not involved in diabetes-accelerated atherosclerosis.

scholarly journals Fulminant Type 1 Diabetes as a Model of Nature to Explore the Role of C-Peptide

2008 ◽  
Vol 2008 ◽  
pp. 1-2
Author(s):  
Yuko Murase-Mishiba ◽  
A. Imagawa ◽  
Toshiaki Hanafusa
Keyword(s):  
Type 1 Diabetes ◽  
Physiological Role ◽  
Chronic Complications ◽  
Fulminant Type 1 Diabetes ◽  
C Peptide ◽  
Onset Of Diabetes ◽  
Fulminant Type

Patients with fulminant type 1 diabetes almost completely lack C-peptide even soon after the onset of the disease, and the deficiency continues for the rest of their life. Thus, fulminant type 1 diabetes could serve as a good model of nature to explore the physiological role of C-peptide. For example, patients with fulminant type 1 diabetes have diabetic chronic complications more frequently than those with classical autoimmune type 1 diabetes 5 years after the onset of diabetes, and the higher prevalence could be partly attributable to the complete lack of C-peptide in fulminant type 1 diabetes.

scholarly journals A Possible Anti-Inflammatory Role of Angiotensin II Type 2 Receptor in Immune-Mediated Glomerulonephritis during Type 1 Receptor Blockade

2006 ◽  
Vol 169 (5) ◽  
pp. 1577-1589 ◽  
Author(s):  
Hirokazu Okada ◽  
Tsutomu Inoue ◽  
Tomohiro Kikuta ◽  
Yusuke Watanabe ◽  
Yoshihiko Kanno ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Receptor Blockade ◽  
Immune Mediated ◽  
Anti Inflammatory

scholarly journals Celiac Disease in Children, Particularly with Accompanying Type 1 Diabetes, Is Characterized by Substantial Changes in the Blood Cytokine Balance, Which May Reflect Inflammatory Processes in the Small Intestinal Mucosa

2019 ◽  
Vol 2019 ◽  
pp. 1-17 ◽  
Author(s):  
Tamara Vorobjova ◽  
Aili Tagoma ◽  
Astrid Oras ◽  
Kristi Alnek ◽  
Kalle Kisand ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Celiac Disease ◽  
Small Bowel ◽  
Inflammatory Response ◽  
Lamina Propria ◽  
Small Bowel Mucosa ◽  
Anti Inflammatory ◽  
Bowel Mucosa

Cytokines play a pivotal role in the maintenance of intestinal homeostasis inducing pro- or anti-inflammatory response and mucosal barrier function in celiac disease (CD) and type 1 diabetes (T1D). We aimed to compare the levels of pro- and anti-inflammatory cytokines in CD patients without and with coexisting T1D, as well as to evaluate its association with the presence of enteroviruses (EV), regulatory T cells (Tregs), and dendritic cells (DCs) in small bowel mucosa. Altogether, 72 patients (median age 10.1 years) who had undergone small bowel biopsy were studied. The study group consisted of 24 patients with CD (median age 6.5 years), 9 patients with CD and concomitant T1D (median age 7.0 years), two patients with T1D (median age 8.5 years), and 37 patients (median age 14.0 years) with functional gastrointestinal disorders (FGD) and a normal small bowel mucosa as controls. The levels of 33 cytokines in serum were measured by multiple analysis using the Milliplex® MAP Magnetic Bead assay. The densities of FOXP3+ Tregs, CD11c+ DC, indoleamine 2,3-dioxygenase+ (IDO+) DC, langerin+ (CD207+) DCs, and EV were evaluated by immunohistochemistry as described in our previous studies. Circulating anti-EV IgA and IgG were evaluated using ELISA. The most important finding of the study is the significant increase of the serum levels of IL-5, IL-8, IL-13, IL-15, IL-17F, IL-22, IL-27, IP-10, MIP-1β, sIL-2Rα, sTNFRII, and TNFαin CD patients compared to controls and its correlation with the degree of small bowel mucosa damage graded according to the Marsh classification. The leptin level was higher in females in all study groups. The levels of IL-2, IL-6, IL-12 (P70), IL-15, IP-10, and IFNγcorrelated significantly with the density of FOXP3+ Tregs inlamina propriaof the small bowel mucosa, which supports the evidence about the signaling role of these cytokines in the peripheral maintenance of FOXP3+ Tregs. At the same time, a significant negative correlation occurred between the level of IL-4 and density of FOXP3+ Tregs in controls. Another important finding of our study was the correlation of IL-17F, IP-10, sTNFRII, MCP-1, and GM-CSF with the density of EV-positive cells in thelamina propriaof the small bowel mucosa. Correlation of MIP-1 (CCL-4) with CD103+ DC and langerin+ DC densities may point to their significance in the recruitment of immune cells into thelamina propriaand in driving the inflammatory response in CD patients. Our results suggest the predominance of Th1 and Th17 immune responses over EV VP1 protein in CD and T1D patients. The significant elevation of Th2 cytokines, like IL-5 and IL-13, but not IL-4, in CD patients and its correlation with the degree of small bowel mucosa damage could reflect the role of these cytokines in gut defense and inflammation.

scholarly journals STRUCTURE, PROPERTIES AND PHYSIOLOGICAL ROLE OF TRPA1 RECEPTORS

2021 ◽  
Vol 67 (1) ◽  
pp. 44-56
Author(s):  
M.A. Petrushenko ◽  
◽  
E.A. Petrushenko ◽  
E.A. Lukyanetz ◽  
◽  
...  
Keyword(s):  
Transient Receptor Potential ◽  
Receptor Gene ◽  
Experimental Studies ◽  
Physiological Role ◽  
Receptor Potential ◽  
Transient Receptor ◽  
Peripheral Sensory ◽  
Structure Properties

In mammals, the ankyrin ionotropic transient receptor potential type 1 (TRPA1) is the only member of the TRPA receptor gene subfamily. It is defined as a target for damaging and inflammatory effects in peripheral sensory neurons, which implies its functional role in the development of pain and neurogenic inflammation. Experimental studies indicate that calcium permeable non-selective ion receptor channel TRPA1 is activated by a number of exogenous irritant compounds, factors including low temperatures. This review describes the structure, properties, and physiological role of TRPA1 receptors.

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