Lysophosphatidic acid (LPA), a small bioactive glycerophospholipid, has been reported to play an indispensable role in the regulation of a wide range of cellular processes, including cell proliferation, morphology, differentiation, invasion, migration, and apoptosis. Besides, it has a diverse role in the development, differentiation, migration, and trafficking of immune cells. The role of LPA in the functioning of immune cells, such as macrophages, natural killer cells, T cells, and B cells has been poorly understood and is still a major thrust area for immunological research. Further, accumulating experimental evidence indicates the pro-tumoral action of LPA in various cancers, including hematological malignancies. Hematological malignancies or blood cancers are a group of neoplastic conditions derived from the cells of hematopoietic tissues. LPA is reported to promote the development and progression of cancers of hematological origin through altering apoptosis, invasion and migration, metabolism, and anti-tumor immune response. But still, the mechanistic pathways by which LPA supports the development and progression of hematological malignancies are not well explored. The present review aims to provide an elaborate survey on the role of LPA in the functioning of immune cells and its implication in hematological malignancies.
{"title":"Role of lysophosphatidic acid in the regulation of immune cells and hematological malignancies","authors":"Vishal Kumar Gupta , Kriti Gupta , Pratishtha Sonker , Manoj Mishra , Ajay Kumar","doi":"10.1016/j.prostaglandins.2025.107028","DOIUrl":"10.1016/j.prostaglandins.2025.107028","url":null,"abstract":"<div><div>Lysophosphatidic acid (LPA), a small bioactive glycerophospholipid, has been reported to play an indispensable role in the regulation of a wide range of cellular processes, including cell proliferation, morphology, differentiation, invasion, migration, and apoptosis. Besides, it has a diverse role in the development, differentiation, migration, and trafficking of immune cells. The role of LPA in the functioning of immune cells, such as macrophages, natural killer cells, T cells, and B cells has been poorly understood and is still a major thrust area for immunological research. Further, accumulating experimental evidence indicates the pro-tumoral action of LPA in various cancers, including hematological malignancies. Hematological malignancies or blood cancers are a group of neoplastic conditions derived from the cells of hematopoietic tissues. LPA is reported to promote the development and progression of cancers of hematological origin through altering apoptosis, invasion and migration, metabolism, and anti-tumor immune response. But still, the mechanistic pathways by which LPA supports the development and progression of hematological malignancies are not well explored. The present review aims to provide an elaborate survey on the role of LPA in the functioning of immune cells and its implication in hematological malignancies.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"180 ","pages":"Article 107028"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144922990","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}
Pub Date : 2025-09-01DOI: 10.1016/j.prostaglandins.2025.107025
Juanjuan Zhu , Bingbing Wang , Sanaz Asemani , Shiwei Bao , Niannian Tian
{"title":"Corrigendum to “The association between vitamin D deficiency and childhood obesity and its impact on children’s serum calcium, alkaline phosphatase, and bone age” [Prostaglandins Other Lipid Mediat. 176 (2024) 106920]","authors":"Juanjuan Zhu , Bingbing Wang , Sanaz Asemani , Shiwei Bao , Niannian Tian","doi":"10.1016/j.prostaglandins.2025.107025","DOIUrl":"10.1016/j.prostaglandins.2025.107025","url":null,"abstract":"","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"180 ","pages":"Article 107025"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668262","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}
Pub Date : 2025-08-22DOI: 10.1016/j.prostaglandins.2025.107026
Yanqiong Shi, Yang Liang, Yang Chen, Zhenghuan Li
Acute lung injury (ALI) is a common disorder of the respiratory system with high mortality. Inducing mitophagy is generally considered to be an effective target for alleviating ALI. We aimed to elucidate the role of immunity related GTPase M (IRGM) in ALI by using a lipopolysaccharide (LPS)-induced alveolar epithelial cell model. Firstly, IRGM expression in A549 cells under LPS conditions was evaluated. Then, IRGM was upregulated and oxidative stress was evaluated by measuring intracellular reactive oxygen species (ROS) using 2′, 7′-Dichlorofluorescin diacetate (DCFH-DA) staining. The permeability of A549 cells was determined by detecting transepithelial electrical resistance (TEER) value and fluorescein isothiocyanate-dextran 4 (FITC-FD4) fluorescence. Proteins related to epithelial barrier, mitophagy and mitochondrial function were assessed. Further Mdivi-1 (an inhibitor of mitophagy) addition or cyclic GMP-AMP synthase (cGAS)- stimulator of interferon genes (STING) signaling overexpression was conducted to investigate the potential mechanism. Results suggested that IRGM was downregulated in LPS-treated A549 cells and IRGM upregulation alleviated LPS-induced oxidative stress, inflammation and barrier dysfunction in A549 cells. IRGM upregulation induced mitophagy and maintains mitochondrial function in LPS-treated A549 cells. Particularly, Mdivi-1 treatment or cGAS overexpression abrogated the impacts of IRGM upregulation on oxidative stress, inflammation and barrier dysfunction in LPS-treated A549 cells. Collectively, IRGM attenuates LPS-triggered alveolar epithelial cell damage by enhancing mitophagy to inactivate cGAS/STING signaling.
急性肺损伤（ALI）是一种常见的呼吸系统疾病，死亡率高。诱导线粒体自噬通常被认为是缓解ALI的有效靶点。我们旨在通过脂多糖（LPS）诱导的肺泡上皮细胞模型阐明免疫相关的GTPase M （IRGM）在ALI中的作用。首先，检测LPS条件下IRGM在A549细胞中的表达。然后，上调IRGM，并通过2 ',7 ' -二氯荧光素双醋酸酯（DCFH-DA）染色测定细胞内活性氧（ROS）来评估氧化应激。通过检测A549细胞上皮电阻值（TEER）和荧光素异硫氰酸酯-葡聚糖4 （FITC-FD4）荧光检测A549细胞的通透性。评估与上皮屏障、线粒体自噬和线粒体功能相关的蛋白。进一步研究Mdivi-1（一种线粒体自噬抑制剂）添加或环GMP-AMP合成酶(cGAS)-干扰素基因（STING）信号过表达刺激因子的潜在机制。结果表明，IRGM在lps处理的A549细胞中下调，IRGM上调可减轻lps诱导的A549细胞氧化应激、炎症和屏障功能障碍。在lps处理的A549细胞中，IRGM上调诱导线粒体自噬并维持线粒体功能。特别是，Mdivi-1处理或cGAS过表达消除了IRGM上调对lps处理的A549细胞氧化应激、炎症和屏障功能障碍的影响。总的来说，IRGM通过增强线粒体自噬使cGAS/STING信号失活来减弱lps触发的肺泡上皮细胞损伤。
{"title":"Role of IRGM in acute lung injury: Inducing mitophagy and inactivating cGAS-STING signaling to improve lipopolysaccharide-induced alveolar epithelial barrier dysfunction","authors":"Yanqiong Shi, Yang Liang, Yang Chen, Zhenghuan Li","doi":"10.1016/j.prostaglandins.2025.107026","DOIUrl":"10.1016/j.prostaglandins.2025.107026","url":null,"abstract":"<div><div>Acute lung injury (ALI) is a common disorder of the respiratory system with high mortality. Inducing mitophagy is generally considered to be an effective target for alleviating ALI. We aimed to elucidate the role of immunity related GTPase M (IRGM) in ALI by using a lipopolysaccharide (LPS)-induced alveolar epithelial cell model. Firstly, IRGM expression in A549 cells under LPS conditions was evaluated. Then, IRGM was upregulated and oxidative stress was evaluated by measuring intracellular reactive oxygen species (ROS) using 2′, 7′-Dichlorofluorescin diacetate (DCFH-DA) staining. The permeability of A549 cells was determined by detecting transepithelial electrical resistance (TEER) value and fluorescein isothiocyanate-dextran 4 (FITC-FD4) fluorescence. Proteins related to epithelial barrier, mitophagy and mitochondrial function were assessed. Further Mdivi-1 (an inhibitor of mitophagy) addition or cyclic GMP-AMP synthase (cGAS)- stimulator of interferon genes (STING) signaling overexpression was conducted to investigate the potential mechanism. Results suggested that IRGM was downregulated in LPS-treated A549 cells and IRGM upregulation alleviated LPS-induced oxidative stress, inflammation and barrier dysfunction in A549 cells. IRGM upregulation induced mitophagy and maintains mitochondrial function in LPS-treated A549 cells. Particularly, Mdivi-1 treatment or cGAS overexpression abrogated the impacts of IRGM upregulation on oxidative stress, inflammation and barrier dysfunction in LPS-treated A549 cells. Collectively, IRGM attenuates LPS-triggered alveolar epithelial cell damage by enhancing mitophagy to inactivate cGAS/STING signaling.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"180 ","pages":"Article 107026"},"PeriodicalIF":2.5,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144893661","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}
Pub Date : 2025-07-15DOI: 10.1016/j.prostaglandins.2025.107024
Mona A. El-Bana , Jihan Hussein , Sherien M. El-Daly , Heba H. Metwaly , Mahmoud A. Abdel-Monem , Enayat A. Omara , Dalia Medhat
This study aimed to investigate brain signaling mechanisms affected by estradiol deficiency during menopause and how these pathways are modified with 17β-estradiol replacement to mitigate menopause-related changes, particularly in cognitive function and neuroinflammation, which are linked to the risk of dementia. Forty female white albino rats were divided into four groups: control, sham, ovariectomized (OVX), and OVX rats treated with 17β-estradiol. Cognitive tests using the Morris Water Maze assessed spatial learning and memory, while neurotransmitter levels were analyzed via HPLC. Serum levels of estrogen, Nerve Growth Factor (NGF), amyloid precursor protein(Aβ), and Postsynaptic Density Protein 95 (PSD-95) were measured using ELISA. Additionally, RT-PCR was used to evaluate the expression of gap junction protein connexin-43 (Cx43), Lipoprotein receptor-related protein (LRP1), and receptor for advanced glycation end products (RAGE), and aromatase expression was assessed via immunohistochemistry. Results showed that estrogen deficiency in OVX rats led to significant impairments in cognition, neurotransmitter signaling, and neurotrophic factors. Reduced NGF and altered PSD-95 levels indicated compromised neuronal health and synaptic plasticity. Increased aromatase expression reflected reduced local estrogen synthesis, potentially contributing to cognitive deficits. Upregulated RAGE and altered LRP1 expression suggested inflammatory and neurodegenerative processes, while decreased Cx43 expression and modified Aβ processing indicated impaired intercellular communication. Overall, the findings highlight the detrimental effects of estrogen deficiency on brain function and suggest that 17β-estradiol replacement may mitigate menopause-related cognitive decline and neuroinflammation.
{"title":"Exploring the diverse signaling mechanisms of 17β-estradiol deficiency and replacement: Impacts on cognitive dysfunction in a post-menopausal experimental model","authors":"Mona A. El-Bana , Jihan Hussein , Sherien M. El-Daly , Heba H. Metwaly , Mahmoud A. Abdel-Monem , Enayat A. Omara , Dalia Medhat","doi":"10.1016/j.prostaglandins.2025.107024","DOIUrl":"10.1016/j.prostaglandins.2025.107024","url":null,"abstract":"<div><div>This study aimed to investigate brain signaling mechanisms affected by estradiol deficiency during menopause and how these pathways are modified with 17β-estradiol replacement to mitigate menopause-related changes, particularly in cognitive function and neuroinflammation, which are linked to the risk of dementia. Forty female white albino rats were divided into four groups: control, sham, ovariectomized (OVX), and OVX rats treated with 17β-estradiol. Cognitive tests using the Morris Water Maze assessed spatial learning and memory, while neurotransmitter levels were analyzed via HPLC. Serum levels of estrogen, Nerve Growth Factor (NGF), amyloid precursor protein(Aβ), and Postsynaptic Density Protein 95 (PSD-95) were measured using ELISA. Additionally, RT-PCR was used to evaluate the expression of gap junction protein connexin-43 (Cx43), Lipoprotein receptor-related protein (LRP1), and receptor for advanced glycation end products (RAGE), and aromatase expression was assessed via immunohistochemistry. Results showed that estrogen deficiency in OVX rats led to significant impairments in cognition, neurotransmitter signaling, and neurotrophic factors. Reduced NGF and altered PSD-95 levels indicated compromised neuronal health and synaptic plasticity. Increased aromatase expression reflected reduced local estrogen synthesis, potentially contributing to cognitive deficits. Upregulated RAGE and altered LRP1 expression suggested inflammatory and neurodegenerative processes, while decreased Cx43 expression and modified Aβ processing indicated impaired intercellular communication. Overall, the findings highlight the detrimental effects of estrogen deficiency on brain function and suggest that 17β-estradiol replacement may mitigate menopause-related cognitive decline and neuroinflammation.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"180 ","pages":"Article 107024"},"PeriodicalIF":2.5,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144660066","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}
Pub Date : 2025-07-01DOI: 10.1016/j.prostaglandins.2025.107011
Rushitha Sadasevevam, Norhaniza Aminudin, Noorlidah Abdullah
Atherosclerosis is an inflammatory condition that contributes to myocardial infarction, cardiac arrest and stroke. Current knowledge of mushroom metabolomics in the context of atherosclerosis remains inadequate. Hence, further investigation into the underlying pathways and characterization of metabolites is necessary to establish a significant network for early-stage diagnosis of atherosclerosis. Therefore, the standard phytopreparation of Schizophyllum commune (SPPSC) was administered in hypercholesterolemic-induced rats. Sera were evaluated for lipid profile parameters; hepatic marker enzymes and the metabolic profile characterization was determined via liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (LC-QTOF-MS). SPPSC suppressed the elevation of cholesterol, LDL, triglyceride and atherogenic coefficient levels while increased HDL concentration and restored the function of hepatic antioxidant enzymes. The predictive accuracies and partial least square discriminant analysis (PLS-DA) revealed clear separation in metabolic features between normal, untreated, olive oil and SPPSC treated groups. Pathway analysis of the most significant metabolites targeted towards anti-atherosclerotic and cardio-protective activities were tryptophan metabolism, sphingolipid metabolism, β-alanine metabolism, taurine and hypotaurine metabolism, glutathione metabolism, phenylalanine metabolism, primary bile acid biosynthesis, histidine metabolism, pantothenate and CoA biosynthesis and cysteine and methionine metabolism. Identified metabolites indicate that S. commune is novel in preventing atherosclerosis and enhancing endogenous antioxidant system, protecting the cardiovascular system, minimalizing inflammation and regulating endothelial dysfunction.
{"title":"Metabolic profiling of bioactive components from Schizophyllum commune Fries in hypercholesterolemic Wistar-Kyoto rats using LC-QTOF-MS analysis","authors":"Rushitha Sadasevevam, Norhaniza Aminudin, Noorlidah Abdullah","doi":"10.1016/j.prostaglandins.2025.107011","DOIUrl":"10.1016/j.prostaglandins.2025.107011","url":null,"abstract":"<div><div>Atherosclerosis is an inflammatory condition that contributes to myocardial infarction, cardiac arrest and stroke. Current knowledge of mushroom metabolomics in the context of atherosclerosis remains inadequate. Hence, further investigation into the underlying pathways and characterization of metabolites is necessary to establish a significant network for early-stage diagnosis of atherosclerosis. Therefore, the standard phytopreparation of <em>Schizophyllum commune</em> (SPPSC) was administered in hypercholesterolemic-induced rats. Sera were evaluated for lipid profile parameters; hepatic marker enzymes and the metabolic profile characterization was determined via liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (LC-QTOF-MS). SPPSC suppressed the elevation of cholesterol, LDL, triglyceride and atherogenic coefficient levels while increased HDL concentration and restored the function of hepatic antioxidant enzymes. The predictive accuracies and partial least square discriminant analysis (PLS-DA) revealed clear separation in metabolic features between normal, untreated, olive oil and SPPSC treated groups. Pathway analysis of the most significant metabolites targeted towards anti-atherosclerotic and cardio-protective activities were tryptophan metabolism, sphingolipid metabolism, β-alanine metabolism, taurine and hypotaurine metabolism, glutathione metabolism, phenylalanine metabolism, primary bile acid biosynthesis, histidine metabolism, pantothenate and CoA biosynthesis and cysteine and methionine metabolism. Identified metabolites indicate that <em>S. commune</em> is novel in preventing atherosclerosis and enhancing endogenous antioxidant system, protecting the cardiovascular system, minimalizing inflammation and regulating endothelial dysfunction.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"179 ","pages":"Article 107011"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144596727","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}
Pub Date : 2025-05-16DOI: 10.1016/j.prostaglandins.2025.106998
Rebecca Kirchhoff, Michel André Chromik, Nils Helge Schebb
Phagocytosis is a key process in human innate immune response. Human macrophages are important phagocytes engulfing and neutralizing pathogens and cell debris. In addition, they modulate the inflammatory process by releasing cytokines and lipid mediators. However, the link between oxylipins and phagocytosis in different macrophage phenotypes remains poorly understood. In order to better understand the link between phagocytosis and the arachidonic acid (ARA) cascade, we established a phagocytosis assay in primary human ‘inflammatory’ M1- and ‘anti-inflammatory’ M2-like macrophages from peripheral blood mononuclear cells (PBMC), representing extremes of macrophage phenotypes. The branches of the ARA cascade were investigated by quantitative targeted proteomics and metabolomics. M1-like macrophages show a higher abundance of cyclooxygenase (COX)-2 and its products particularly after LPS stimulus compared to M2-like macrophages. LPS increased phagocytosis in M2-like, but not in M1-like macrophages. We demonstrate that the COX product prostaglandin E2 (PGE2) modulates the differential effects of LPS on phagocytosis: Via the EP4 receptor PGE2 signaling suppresses phagocytosis in primary human macrophages. Thus, blockage of COX, e.g. by non-steroidal anti-inflammatory drugs (NSAID), leads to an increase of phagocytosis also in ‘inflammatory’ M1-like macrophages. This supports the well-described anti-inflammatory effects of these drugs and underscores the importance of the link between the COX branch of the ARA cascade and the regulation of phagocytosis in human macrophages.
{"title":"Phagocytosis is differentially regulated by LPS in M1- and M2-like macrophages via PGE2 formation and EP4 signaling","authors":"Rebecca Kirchhoff, Michel André Chromik, Nils Helge Schebb","doi":"10.1016/j.prostaglandins.2025.106998","DOIUrl":"10.1016/j.prostaglandins.2025.106998","url":null,"abstract":"<div><div>Phagocytosis is a key process in human innate immune response. Human macrophages are important phagocytes engulfing and neutralizing pathogens and cell debris. In addition, they modulate the inflammatory process by releasing cytokines and lipid mediators. However, the link between oxylipins and phagocytosis in different macrophage phenotypes remains poorly understood. In order to better understand the link between phagocytosis and the arachidonic acid (ARA) cascade, we established a phagocytosis assay in primary human ‘inflammatory’ M1- and ‘anti-inflammatory’ M2-like macrophages from peripheral blood mononuclear cells (PBMC), representing extremes of macrophage phenotypes. The branches of the ARA cascade were investigated by quantitative targeted proteomics and metabolomics. M1-like macrophages show a higher abundance of cyclooxygenase (COX)-2 and its products particularly after LPS stimulus compared to M2-like macrophages. LPS increased phagocytosis in M2-like, but not in M1-like macrophages. We demonstrate that the COX product prostaglandin E2 (PGE<sub>2</sub>) modulates the differential effects of LPS on phagocytosis: Via the EP4 receptor PGE<sub>2</sub> signaling suppresses phagocytosis in primary human macrophages. Thus, blockage of COX, e.g. by non-steroidal anti-inflammatory drugs (NSAID), leads to an increase of phagocytosis also in ‘inflammatory’ M1-like macrophages. This supports the well-described anti-inflammatory effects of these drugs and underscores the importance of the link between the COX branch of the ARA cascade and the regulation of phagocytosis in human macrophages.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"178 ","pages":"Article 106998"},"PeriodicalIF":2.5,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144094230","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}
Pub Date : 2025-05-14DOI: 10.1016/j.prostaglandins.2025.106997
Liming Wang, Yan Yang, Haibing Sun, Mengxue Fei
Background
Nonalcoholic fatty liver disease (NAFLD) is a prevalent liver condition associated with metabolic syndrome, often aggravated by inflammation and mitochondrial dysfunction. This study aims to explore the therapeutic potential of magnoflorine, an alkaloid with known anti-inflammatory properties, in ameliorating NAFLD by modulating mitochondrial autophagy and inhibiting the NLRP3 inflammasome.
Methods
Male C57BL/6 J mice were fed a high-fat diet (HFD) for 16 weeks to induce NAFLD. Magnoflorine (5 and 10 mg/kg) was administered by gavage daily for 16 weeks. Liver and serum samples were analyzed for lipid profiles, inflammation markers, and autophagy-related proteins, and liver histology was examined to assess changes.
Results
Magnoflorine treatment improved dyslipidemia in NAFLD mice, shown by decreased serum triglycerides, total cholesterol, and LDL-C, and increased HDL-C. Histological analysis showed reduced hepatic steatosis and inflammation, with less lipid droplet accumulation and hepatocyte ballooning. Western blot results indicated upregulation of Parkin and PINK1, and downregulation of NLRP3, ASC, and caspase-1, with lower serum IL-1β levels, reflecting reduced inflammation.
Conclusions
Magnoflorine offers a promising approach for mitigating NAFLD progression through modulating mitochondrial autophagy and inhibiting inflammation.
{"title":"Magnoflorine alleviates nonalcoholic fatty liver disease by modulating lipid metabolism, mitophagy and inflammation","authors":"Liming Wang, Yan Yang, Haibing Sun, Mengxue Fei","doi":"10.1016/j.prostaglandins.2025.106997","DOIUrl":"10.1016/j.prostaglandins.2025.106997","url":null,"abstract":"<div><h3>Background</h3><div>Nonalcoholic fatty liver disease (NAFLD) is a prevalent liver condition associated with metabolic syndrome, often aggravated by inflammation and mitochondrial dysfunction. This study aims to explore the therapeutic potential of magnoflorine, an alkaloid with known anti-inflammatory properties, in ameliorating NAFLD by modulating mitochondrial autophagy and inhibiting the NLRP3 inflammasome.</div></div><div><h3>Methods</h3><div>Male C57BL/6 J mice were fed a high-fat diet (HFD) for 16 weeks to induce NAFLD. Magnoflorine (5 and 10 mg/kg) was administered by gavage daily for 16 weeks. Liver and serum samples were analyzed for lipid profiles, inflammation markers, and autophagy-related proteins, and liver histology was examined to assess changes.</div></div><div><h3>Results</h3><div>Magnoflorine treatment improved dyslipidemia in NAFLD mice, shown by decreased serum triglycerides, total cholesterol, and LDL-C, and increased HDL-C. Histological analysis showed reduced hepatic steatosis and inflammation, with less lipid droplet accumulation and hepatocyte ballooning. Western blot results indicated upregulation of Parkin and PINK1, and downregulation of NLRP3, ASC, and caspase-1, with lower serum IL-1β levels, reflecting reduced inflammation.</div></div><div><h3>Conclusions</h3><div>Magnoflorine offers a promising approach for mitigating NAFLD progression through modulating mitochondrial autophagy and inhibiting inflammation.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"178 ","pages":"Article 106997"},"PeriodicalIF":2.5,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086310","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}
Pub Date : 2025-05-07DOI: 10.1016/j.prostaglandins.2025.106996
Yangli Pei, Siyu Wu, Zheng Feng
Lipid droplets (LDs) are essential intracellular organelles involved in lipid storage and metabolism, playing critical roles in various cellular processes and diseases. Researchers require efficiently isolate and analyze LDs to understand lipid metabolism and related pathologies. This review summarizes recent advances in LD isolation methods, including traditional techniques such as centrifugation and density gradient centrifugation, as well as emerging technologies like automated and high-throughput approaches. We explore the applications of these methods in lipid metabolism research and discuss the challenges faced by current isolation techniques. Future directions, including automation, single-cell analysis, and integration with advanced analytical tools, are also highlighted to provide insights for the next generation of LD research.
{"title":"Advances and challenges in lipid droplet isolation from animal tissues and cells","authors":"Yangli Pei, Siyu Wu, Zheng Feng","doi":"10.1016/j.prostaglandins.2025.106996","DOIUrl":"10.1016/j.prostaglandins.2025.106996","url":null,"abstract":"<div><div>Lipid droplets (LDs) are essential intracellular organelles involved in lipid storage and metabolism, playing critical roles in various cellular processes and diseases. Researchers require efficiently isolate and analyze LDs to understand lipid metabolism and related pathologies. This review summarizes recent advances in LD isolation methods, including traditional techniques such as centrifugation and density gradient centrifugation, as well as emerging technologies like automated and high-throughput approaches. We explore the applications of these methods in lipid metabolism research and discuss the challenges faced by current isolation techniques. Future directions, including automation, single-cell analysis, and integration with advanced analytical tools, are also highlighted to provide insights for the next generation of LD research.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"178 ","pages":"Article 106996"},"PeriodicalIF":2.5,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143923469","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}
Pub Date : 2025-04-24DOI: 10.1016/j.prostaglandins.2025.106995
Ibrahim Aktas , Fatih Mehmet Gur , Sedat BILGIÇ
Objective
A major challenge in cancer treatment is the detrimental effects of anticancer drugs on healthy organs and tissues. This study aims to investigate the protective effects of Lutein (LU) against Cisplatin (CT)-induced toxicity in rat liver, utilizing biochemical and histopathological assessments.
Methods
In this study, CT was administered intraperitoneally (i.p.) at a dose of 10 mg/kg, while LU was administered orally at a dose of 100 mg/kg. The experiment was conducted over a 7-day period with 28 male Sprague-Dawley rats (weighing 210–265 g, aged 11 weeks), divided into four groups (n = 7): Control, LU, CT, and CT + LU.
Results
CT-induced liver injury was identified as a dose-limiting side effect of CT. Compared to the CT group, the CT + LU group exhibited a significant decrease in malondialdehyde (MDA) levels and an increase in superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) levels. In the CT group, a significant increase in the levels of gamma-glutamyl transferase (GGT), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) was observed, compared to the control group (p < 0.05). When comparing the CT + LU group with the CT group, a significant reduction in the levels of GGT, ALT, AST, and LDH was observed (p < 0.05). Histopathological analysis revealed liver damage in the CT group, characterized by leukocyte infiltration, sinusoidal dilatation, Councilman body formation, and hepatocellular degeneration and steatosis. In contrast, the CT + LU group exhibited only mild sinusoidal dilatation, with no other significant lesions. Immunohistochemical analysis showed positive staining for tumour necrosis factor-alpha (TNF-α) and caspase-3 in the liver tissue of CT group rats, which was significantly reduced in the CT + LU group. The staining pattern in the CT + LU group was similar to that of the control and LU groups.
Conclusion
The results of this study suggest that LU mitigates oxidative stress, enhances antioxidant defences, and supports liver function. Furthermore, LU demonstrates a protective effect against CT-induced liver damage, indicating its potential as a pharmacological agent for preventing CT-induced hepatic injury.
{"title":"Protection of lutein against the toxic effect of cisplatin on liver in male rat","authors":"Ibrahim Aktas , Fatih Mehmet Gur , Sedat BILGIÇ","doi":"10.1016/j.prostaglandins.2025.106995","DOIUrl":"10.1016/j.prostaglandins.2025.106995","url":null,"abstract":"<div><h3>Objective</h3><div>A major challenge in cancer treatment is the detrimental effects of anticancer drugs on healthy organs and tissues. This study aims to investigate the protective effects of Lutein (LU) against Cisplatin (CT)-induced toxicity in rat liver, utilizing biochemical and histopathological assessments.</div></div><div><h3>Methods</h3><div>In this study, CT was administered intraperitoneally (i.p.) at a dose of 10 mg/kg, while LU was administered orally at a dose of 100 mg/kg. The experiment was conducted over a 7-day period with 28 male Sprague-Dawley rats (weighing 210–265 g, aged 11 weeks), divided into four groups (n = 7): Control, LU, CT, and CT + LU.</div></div><div><h3>Results</h3><div>CT-induced liver injury was identified as a dose-limiting side effect of CT. Compared to the CT group, the CT + LU group exhibited a significant decrease in malondialdehyde (MDA) levels and an increase in superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) levels. In the CT group, a significant increase in the levels of gamma-glutamyl transferase (GGT), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) was observed, compared to the control group (p < 0.05). When comparing the CT + LU group with the CT group, a significant reduction in the levels of GGT, ALT, AST, and LDH was observed (p < 0.05). Histopathological analysis revealed liver damage in the CT group, characterized by leukocyte infiltration, sinusoidal dilatation, Councilman body formation, and hepatocellular degeneration and steatosis. In contrast, the CT + LU group exhibited only mild sinusoidal dilatation, with no other significant lesions. Immunohistochemical analysis showed positive staining for tumour necrosis factor-alpha (TNF-α) and caspase-3 in the liver tissue of CT group rats, which was significantly reduced in the CT + LU group. The staining pattern in the CT + LU group was similar to that of the control and LU groups.</div></div><div><h3>Conclusion</h3><div>The results of this study suggest that LU mitigates oxidative stress, enhances antioxidant defences, and supports liver function. Furthermore, LU demonstrates a protective effect against CT-induced liver damage, indicating its potential as a pharmacological agent for preventing CT-induced hepatic injury.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"178 ","pages":"Article 106995"},"PeriodicalIF":2.5,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143874115","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}
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