Prostaglandins & other lipid mediators最新文献

{"title":"PGC-1α inhibits NLRP3 signaling through transcriptional activation of POP1 to alleviate inflammation and strengthen osteogenic differentiation of lipopolysaccharide-induced human periodontal stem cells","authors":"Fuying Liang ,&nbsp;Shanshan Huang","doi":"10.1016/j.prostaglandins.2024.106853","DOIUrl":"10.1016/j.prostaglandins.2024.106853","url":null,"abstract":"<div><p>Periodontitis is a chronic infectious disease that affects the oral health of adults. Periodontal stem cells (PDLSCs) have good self-renewal and multipotential differentiation abilities to maintain the integrity of periodontal support structure and repair defects. This study aimed to elucidate the role of peroxisome proliferator activated receptor-γ co-activator 1-α (PGC-1α) in lipopolysaccharide (LPS)-induced PDLSCs and the underlying mechanisms related to predicated that pyrin domain (PYD)-only protein 1 (POP1). Notably downregulated PGC-1α and POP1 expression was observed in LPS-induced PDLSCs. PGC-1α or POP1 overexpression significantly reduced the inflammation and enhanced the osteogenic differentiation of LPS-treated PDLSCs. Particularly, PGC-1 bound to POP1 promoter region and upregulated POP1 expression. Moreover, POP1 knockdown ameliorated the impacts of PGC-1α overexpression on the inflammation and osteogenic differentiation in LPS-induced PDLSCs. Besides, PGC-1α inactivated NLRP3 signaling in LPS-treated PDLSCs, which was reversed by POP1 knockdown. Taken together, PGC-1α inhibits NLRP3 signaling through transcriptional activation of POP1, thereby alleviating inflammation and strengthening osteogenic differentiation of LPS-induced PDLSCs.</p></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"174 ","pages":"Article 106853"},"PeriodicalIF":2.9,"publicationDate":"2024-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141043844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Changes in cardiovascular arachidonic acid metabolism in experimental models of menopause and implications on postmenopausal cardiac hypertrophy","authors":"Samar H. Gerges,&nbsp;Ayman O.S. El-Kadi","doi":"10.1016/j.prostaglandins.2024.106851","DOIUrl":"10.1016/j.prostaglandins.2024.106851","url":null,"abstract":"<div><p>Menopause is a normal stage in the human female aging process characterized by the cessation of menstruation and the ovarian production of estrogen and progesterone hormones. Menopause is associated with an increased risk of several different diseases. Cardiovascular diseases are generally less common in females than in age-matched males. However, this female advantage is lost after menopause. Cardiac hypertrophy is a disease characterized by increased cardiac size that develops as a response to chronic overload or stress. Similar to other cardiovascular diseases, the risk of cardiac hypertrophy significantly increases after menopause. However, the exact underlying mechanisms are not yet fully elucidated. Several studies have shown that surgical or chemical induction of menopause in experimental animals is associated with cardiac hypertrophy, or aggravates cardiac hypertrophy induced by other stressors. Arachidonic acid (AA) released from the myocardial phospholipids is metabolized by cardiac cytochrome P450 (CYP), cyclooxygenase (COX), and lipoxygenase (LOX) enzymes to produce several eicosanoids. AA-metabolizing enzymes and their respective metabolites play an important role in the pathogenesis of cardiac hypertrophy. Menopause is associated with changes in the cardiovascular levels of CYP, COX, and LOX enzymes and the levels of their metabolites. It is possible that these changes might play a role in the increased risk of cardiac hypertrophy after menopause.</p></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"173 ","pages":"Article 106851"},"PeriodicalIF":2.9,"publicationDate":"2024-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1098882324000455/pdfft?md5=db3c6b155f60db3cd67bf382d758af8e&pid=1-s2.0-S1098882324000455-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140916790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Soluble epoxide hydrolase inhibition reverses cognitive dysfunction in a mouse model of metabolic syndrome by modulating inflammation","authors":"Thierno M. Bah ,&nbsp;Catherine M. Davis ,&nbsp;Elyse M. Allen ,&nbsp;Rohan N. Borkar ,&nbsp;Ruby Perez ,&nbsp;Marjorie R. Grafe ,&nbsp;Jacob Raber ,&nbsp;Martin M. Pike ,&nbsp;Nabil J. Alkayed","doi":"10.1016/j.prostaglandins.2024.106850","DOIUrl":"10.1016/j.prostaglandins.2024.106850","url":null,"abstract":"<div><p>Midlife metabolic syndrome (MetS) is associated with cognitive impairment in late life. The mechanism of delayed MetS-related cognitive dysfunction (MetSCD) is not clear, but it has been linked to systemic inflammation and chronic cerebral microangiopathy. Currently there is no treatment for late life MetSCD other than early risk factor modification. We investigated the effect of soluble epoxide hydrolase (sEH) inhibitor 4-[[<em>trans</em>-4-[[(tricyclo[3.3.1.13,7]dec-1-ylamino)carbonyl]amino]cyclohexyl]oxy]-benzoic acid (t-AUCB) on cognitive performance, cerebral blood flow (CBF), and central and peripheral inflammation in the high-fat diet (HFD) model of MetS in mice. At 6 weeks of age, male mice were randomly assigned to receive either HFD or standard chow (STD) for 6 months. Mice received either t-AUCB or vehicle for 4 weeks. Cognitive performance was evaluated, followed by CBF measurement using magnetic resonance imaging (MRI). At the end of the study, blood was collected for measurement of eicosanoids and inflammatory cytokines. The brains were then analyzed by immunohistochemistry for glial activation markers. The HFD caused a significant impairment in novel object recognition. Treatment with t-AUCB increased plasma levels of 14,15-EET, prevented this cognitive impairment and modified hippocampal glial activation and plasma cytokine levels, without affecting CBF in mice on HFD. In conclusion, sEH inhibition for four weeks prevents cognitive deficits in mice on chronic HFD by modulating inflammatory processes without affecting CBF.</p></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"173 ","pages":"Article 106850"},"PeriodicalIF":2.9,"publicationDate":"2024-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140912704","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Platelets and extracellular vesicles in disease promotion via cellular cross-talk and eicosanoid biosynthesis","authors":"Annalisa Contursi ,&nbsp;Stefania Tacconelli ,&nbsp;Sara Di Berardino ,&nbsp;Alessandra De Michele ,&nbsp;Paola Patrignani","doi":"10.1016/j.prostaglandins.2024.106848","DOIUrl":"10.1016/j.prostaglandins.2024.106848","url":null,"abstract":"<div><p>New insights have been gained on the role of platelets beyond thrombosis. Platelets can accumulate in damaged and inflamed tissues, acting as a sentinel to detect and repair tissue damage. However, by releasing several soluble factors, including thromboxane A₂ (TXA₂) and 12-hydroxyeicosatetraenoic acid, and extracellular vesicles (EVs), platelets can activate vascular cells, stromal, such as fibroblasts, immune cells, and cancer cells, leading to atherosclerosis, vascular restenosis, tissue fibrosis, and tumor metastasis. Platelet-derived extracellular vesicles (PEVs) are released when platelets are activated and can transfer their cargo to other cell types, thus contributing to the development of diseases. Inhibitors of the internalization of PEVs can potentially represent novel therapeutic tools. Both platelets and PEVs contain a significant number of different types of molecules, and their omics assessment and integration with clinical data using computational approaches have the potential to detect early disease development and monitor drug treatments.</p></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"173 ","pages":"Article 106848"},"PeriodicalIF":2.9,"publicationDate":"2024-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S109888232400042X/pdfft?md5=4e3e0cad97e751a2ff6bfb5f9a8809c7&pid=1-s2.0-S109888232400042X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140898399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Real time changes in the expression of eicosanoid synthesizing enzymes during inflammation","authors":"Hannah C. Huff ,&nbsp;Justin S. Kim ,&nbsp;Abhishek Ojha ,&nbsp;Saurabh Sinha ,&nbsp;Aditi Das","doi":"10.1016/j.prostaglandins.2024.106839","DOIUrl":"10.1016/j.prostaglandins.2024.106839","url":null,"abstract":"<div><p>Immune responses during inflammation involve complex, well-coordinated lipid signaling pathways. Eicosanoids are a class of lipid signaling molecules derived from polyunsaturated fatty acids such as arachidonic acid and constitute a major network that controls inflammation and its subsequent resolution. Arachidonic acid is metabolized by enzymes in three different pathways to form a variety of lipid metabolites that can be either pro- or anti-inflammatory. Therefore, an understanding of the time-dependent gene expression, lipid metabolite profiles and cytokine profiles during the initial inflammatory response is necessary, as it will allow for the design of time-dependent therapeutics. Herein, we investigate the multi-level regulation of this process. After stimulating RAW 264.7 cells, a mouse-derived macrophage cell line commonly used to examine inflammatory responses, we examine the gene expression of 44 relevant lipid metabolizing enzymes from the different eicosanoid synthesizing classes. We also measure the formation of lipid metabolites and production of cytokines at selected time points. Results reveal a dynamic relationship between the time-course of inflammation dependent gene expression of the three eicosanoid synthesizing enzymes.</p></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"174 ","pages":"Article 106839"},"PeriodicalIF":2.9,"publicationDate":"2024-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140868168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of flaxseed supplementation on lipid profile and liver enzymes in patients with non-alcoholic fatty liver disease: Systematic review and meta-analysis of randomized controlled trials","authors":"Dyari H. Ahmed ,&nbsp;Hawal Lateef Fateh","doi":"10.1016/j.prostaglandins.2024.106838","DOIUrl":"10.1016/j.prostaglandins.2024.106838","url":null,"abstract":"<div><p>Since the effects of flaxseed supplementation on lipid profile and liver enzymes are still controversial, a meta-analysis of randomized controlled trials was conducted in the present study to assess the effect of flaxseed supplementation on lipid profile and liver enzymes. The study was designed, conducted, and reported according to the guidelines of the 2020 preferred reporting items for systematic reviews and meta-analysis (PRISMA) statement. A systematic and comprehensive search was performed in several databases from inception up to January 10, 2024. The meta-analysis on the impact of flaxseed supplementation on lipid profile and liver enzymes indicates that the overall effect of flaxseed supplementation on triglycerides, combining different doses, revealed a significant reduction with a WMD of − 230.72 (-53.95, − 27.49) and a P-value of 0.010. High-density lipoprotein (HDL) demonstrated a positive effect, with an overall WMD of 1.82 (0.27, 3.38) and a P-value of 0.021, indicating an increase in HDL levels. The liver enzymes AST and ALT displayed reductions in their levels, with overall WMDs of − 21.18 (-2.95, 0.59) and − 24.83 (-8.74, − 20.91), respectively. Subgroup analysis based on dosage revealed more pronounced reductions in ALT levels for doses below 2000 mg/day. Findings from this study suggest that a flaxseed supplement might be beneficial to modulate the blood lipid profile and liver enzymes.</p></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"173 ","pages":"Article 106838"},"PeriodicalIF":2.9,"publicationDate":"2024-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140773449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pomegranate seed oil alleviates colitis: Therapeutic effects achieved by modulation of oxidative stress and inflammation in a rat model","authors":"Açelya Gül Koyuncu ,&nbsp;Alev Cumbul ,&nbsp;Muge Kopuz Alvarez Noval ,&nbsp;Elvan Yilmaz Akyüz","doi":"10.1016/j.prostaglandins.2024.106837","DOIUrl":"https://doi.org/10.1016/j.prostaglandins.2024.106837","url":null,"abstract":"<div><p>Pomegranate seed oil shows positive effects by limiting neutrophil activation and lipid peroxidation through its antioxidant and anti-inflammatory activities. This study evaluated the possible ameliorative effects of pomegranate seed oil, its actions on proinflammatory cytokines, and its antioxidant activity using an acute acetic acid-induced colitis model in rats. 32 male Sprague-Dawley rats were divided into 4 groups: control, colitis, 0.4 ml/kg, and 0.8 ml/kg pomegranate seed oil treatment after colitis. At the end of the experiment, histopathological and biochemical analyses of intestinal tissues and blood were performed. The study revealed that administering different doses of pomegranate seed oil dramatically reduced total oxidant levels, nuclear factor kappa B, proinflammatory cytokines, and myeloperoxidase activity and appreciably reduced colitis injury. These findings suggest that pomegranate seed oil may alleviate colitis symptoms effectively and exert protective effects through antioxidant, anti-inflammatory mechanisms.</p></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"173 ","pages":"Article 106837"},"PeriodicalIF":2.9,"publicationDate":"2024-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140641035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A high seizure burden increases several prostaglandin species in the hippocampus of a Scn1a+/- mouse model of Dravet syndrome","authors":"Cilla Zhou ,&nbsp;Vaishali Satpute ,&nbsp;Ka Lai Yip ,&nbsp;Lyndsey L. Anderson ,&nbsp;Nicole Hawkins ,&nbsp;Jennifer Kearney ,&nbsp;Jonathon C. Arnold","doi":"10.1016/j.prostaglandins.2024.106836","DOIUrl":"https://doi.org/10.1016/j.prostaglandins.2024.106836","url":null,"abstract":"<div><p>Dravet syndrome is an intractable epilepsy with a high seizure burden that is resistant to current anti-seizure medications. There is evidence that neuroinflammation plays a role in epilepsy and seizures, however few studies have specifically examined neuroinflammation in Dravet syndrome under conditions of a higher seizure burden. Here we used an established genetic mouse model of Dravet syndrome (<em>Scn1a</em>^<em>+/-</em> mice), to examine whether a higher seizure burden impacts the number and morphology of microglia in the hippocampus. Moreover, we examined whether a high seizure burden influences classical inflammatory mediators in this brain region. <em>Scn1a</em>^<em>+/-</em> mice with a high seizure burden induced by thermal priming displayed a localised reduction in microglial cell density in the granule cell layer and subgranular zone of the dentate gyrus, regions important to postnatal neurogenesis. However, microglial cell number and morphology remained unchanged in other hippocampal subfields. The high seizure burden in <em>Scn1a</em>^<em>+/-</em> mice did not affect hippocampal mRNA expression of classical inflammatory mediators such as interleukin 1β and tumour necrosis factor α, but increased cyclooxygenase 2 (COX-2) expression. We then quantified hippocampal levels of prostanoids that arise from COX-2 mediated metabolism of fatty acids and found that <em>Scn1a</em>^<em>+/-</em> mice with a high seizure burden displayed increased hippocampal concentrations of numerous prostaglandins, notably PGF_2α, PGE₂, PGD₂, and 6-K-PGF_1A, compared to <em>Scn1a</em>^<em>+/-</em> mice with a low seizure burden. In conclusion, a high seizure burden increased hippocampal concentrations of various prostaglandin mediators in a mouse model of Dravet syndrome. Future studies could interrogate the prostaglandin pathways to further better understand their role in the pathophysiology of Dravet syndrome.</p></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"172 ","pages":"Article 106836"},"PeriodicalIF":2.9,"publicationDate":"2024-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140543761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial – Special issue of the 8th European Workshop on Lipid Mediators","authors":"Giulio G. Muccioli ,&nbsp;Gerard Bannenberg","doi":"10.1016/j.prostaglandins.2024.106835","DOIUrl":"10.1016/j.prostaglandins.2024.106835","url":null,"abstract":"","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"172 ","pages":"Article 106835"},"PeriodicalIF":2.9,"publicationDate":"2024-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140332017","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"25-hydroxycholesterol triggers antioxidant signaling in mouse atria","authors":"Julia G. Odnoshivkina ,&nbsp;Alexey M. Petrov","doi":"10.1016/j.prostaglandins.2024.106834","DOIUrl":"https://doi.org/10.1016/j.prostaglandins.2024.106834","url":null,"abstract":"<div><p>Oxysterol, 25-hydroxycholesterol (25HC), is a potent regulator of immune reactions, its synthesis greatly increases by macrophages during inflammation. We hypothesize that 25HC can have cardioprotective effects by limiting consequences of excessive β-adrenoceptor (βAR) stimulation, particularly reactive oxygen species (ROS) production, in mouse atria. Isoproterenol, a βAR agonist, increased extra- and intracellular levels of ROS. This enhancement of ROS production was suppressed by NADPH oxidase antagonists as well as 25HC. Inhibition of β3ARs, Gi protein and protein kinase Cε prevented the effect of 25HC on isoproterenol-dependent ROS synthesis. Furthermore, 25HC suppressed isoproterenol-induced lipid peroxidation and mitochondrial ROS generation as well as ROS-dependent component of positive inotropic response to isoproterenol. Additionally, 25HC decreased mitochondrial ROS production and lipid peroxidation induced by antimycin A, a mitochondrial poison. Thus, 25HC exerts antioxidant properties alleviating mitochondrial dysfunction-induced and βAR-dependent cardiac oxidative damage. In the latter case, 25HC can act via signaling mechanism engaging β3ARs, Gi protein and protein kinase Cε.</p></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"172 ","pages":"Article 106834"},"PeriodicalIF":2.9,"publicationDate":"2024-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140191217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}