Prostaglandins & other lipid mediators最新文献

{"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}

{"title":"Anti-inflammatory actions of aspirin-triggered resolvin D1 (AT-RvD1) in bronchial epithelial cells stimulated by cigarette smoke extract","authors":"Jhony Robson de Oliveira ,&nbsp;Aline Beatriz Mahler Pereira ,&nbsp;Henrique Ismarsi de Souza ,&nbsp;Wanessa Maria dos Santos ,&nbsp;Thaís Sorares Farnesi de Assunção ,&nbsp;Fernanda Bernadelli de Vito ,&nbsp;Helio Moraes de Souza ,&nbsp;Paulo Roberto da Silva ,&nbsp;Marcos Vinicius da Silva ,&nbsp;Virmondes Rodrigues Junior ,&nbsp;Alexandre Paula Rogerio","doi":"10.1016/j.prostaglandins.2024.106833","DOIUrl":"10.1016/j.prostaglandins.2024.106833","url":null,"abstract":"<div><p>Smoking causes several diseases such as chronic obstructive pulmonary disease (COPD). Aspirin-triggered-resolvin D1 (AT-RvD1) is a lipid mediator produced during the resolution of inflammation and demonstrates anti-inflammatory and pro-resolution effects in several inflammatory experimental models including in the airways. Here we evaluated the role of AT-RvD1 (100 nM) in bronchial epithelial cells (BEAS-2B) stimulated by cigarette smoke extract (CSE; 1%; 1 cigarette) for 24 h. CSE induced the productions of IL-1β, TNF-α, IL-10, IL-4 and IFN-γ as well as the activations of NF-κB and STAT3 and the expression of ALX/FPR2 receptor. AT-RvD1 reduced the IL-1β and TNF-α production and increased the production of IFN-γ. These effects were reversed BOC2, an antagonist of ALX/FPR2 receptor for AT-RvD1. The production of IL-4 and IL-10 were not altered by AT-RvD1. In addition, AT-RvD1 reduced the phosphorylation of NF-κB and STAT3 when compared to CSE-stimulated BEAS-2B cells. No alteration of ALX/FPR2 expression was observed by AT-RvD1 when compared to CSE group. In the human monocytic leukemia cell line, the relative number of copies of IL-1β and IL-4 was significantly higher in CSE + AT-RvD1 group compared CSE group, however, the expression of M1 cytokine was more pronounced than M2 profile. AT-RvD1 could be an important target for the reduction of inflammation in the airways associated with smoking.</p></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"172 ","pages":"Article 106833"},"PeriodicalIF":2.9,"publicationDate":"2024-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140068670","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":"IGF2BP3 stabilizes SESN1 mRNA to mitigate oxidized low-density lipoprotein-induced oxidative stress and endothelial dysfunction in human umbilical vein endothelial cells by activating Nrf2 signaling","authors":"Feng Gao,&nbsp;Bin Zhang,&nbsp;Chunwei Xiao,&nbsp;Zhanfa Sun,&nbsp;Yuan Gao,&nbsp;Chunyi Liu,&nbsp;Xueyong Dou,&nbsp;Haokun Tong,&nbsp;Rui Wang,&nbsp;Peng Li,&nbsp;Lei Heng","doi":"10.1016/j.prostaglandins.2024.106832","DOIUrl":"10.1016/j.prostaglandins.2024.106832","url":null,"abstract":"<div><p>Atherosclerosis (AS) represents a prevalent initiating factor for cardiovascular events. Insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3) is an oncofetal RNA-binding protein that participates in cardiovascular diseases. This work aimed to elaborate the effects of IGF2BP3 on AS and the probable mechanism by using an oxidized low-density lipoprotein (ox-LDL)-induced human umbilical vein endothelial cells (HUVECs) model. Results indicated that IGF2BP3 expression was declined in the blood of AS patients and ox-LDL-induced HUVECs. IGF2BP3 elevation alleviated ox-LDL-provoked viability loss, apoptosis, oxidative DNA damage and endothelial dysfunction in HUVECs. Moreover, IGF2BP3 bound SESN1 and stabilized SESN1 mRNA. Furthermore, SESN1 interference reversed the impacts of IGF2BP3 overexpression on the apoptosis, oxidative DNA damage and endothelial dysfunction of ox-LDL-challenged HUVECs. Additionally, the activation of Nrf2 signaling mediated by IGF2BP3 up-regulation in ox-LDL-treated HUVECs was blocked by SESN1 absence. Collectively, SESN1 stabilized by IGF2BP3 might protect against AS by activating Nrf2 signaling.</p></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"172 ","pages":"Article 106832"},"PeriodicalIF":2.9,"publicationDate":"2024-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140068671","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":"The effect of plasma cytokines on the expression of adiponectin and its receptors in the synovial membrane of joints and the infrapatellar fat pad in patients with rheumatoid arthritis and osteoarthritis","authors":"Michał Czerewaty ,&nbsp;Małgorzata Łączna ,&nbsp;Kajetan Kiełbowski ,&nbsp;Estera Bakinowska ,&nbsp;Paweł Dec ,&nbsp;Andrzej Modrzejewski ,&nbsp;Daniel Kotrych ,&nbsp;Piotr Burszewski ,&nbsp;Krzysztof Safranow ,&nbsp;Andrzej Pawlik","doi":"10.1016/j.prostaglandins.2024.106824","DOIUrl":"10.1016/j.prostaglandins.2024.106824","url":null,"abstract":"<div><h3>Background</h3><p>Rheumatoid arthritis (RA) is an autoimmune inflammatory disease that leads to joint destruction. Numerous pro-inflammatory mediators, including adipokines, play an important role in the pathogenesis of RA.</p></div><div><h3>Objective</h3><p>The aim of the study was to investigate the relationships between selected plasma cytokines and expression of adiponectin and its receptors in the synovium and the infrapatellar fat pad in patients with RA and osteoarthritis (OA).</p></div><div><h3>Methods</h3><p>Blood, synovium and fat pad samples from 18 patients with RA and 18 with OA were collected during joint replacement surgery. Spearman rank correlations between plasma concentrations of selected cytokines (IL-1β, IL-2, IL-4, IL-6, IL-7, IL-8, IL-10, IL-12 p40, IL-13, IL-17, G-CSF and GM-CSF) and the expression of adiponectin and its receptors were determined. Plasma levels of cytokines were determined using a magnetic bead-based multiplex assay, mRNA expression of adiponectin and its receptors were determined by real-time PCR.</p></div><div><h3>Results</h3><p>In OA patients, there were significant positive correlations between adiponectin expression in the synovial membrane and plasma levels of IL-1β, IL-4, G-CSF and GM-CSF, as well as a significant positive correlation between adiponectin expression in the fat pad and plasma levels of GM-CSF. In addition, OA patients showed significant negative correlations between AdipoR1 and AdipoR2 expression in the synovial membrane and plasma IL-6 levels, as well as between AdipoR2 expression in the synovial membrane and plasma MCP-1 and TNF-α levels. In patients with RA, there were no significant correlations between adiponectin expression in the synovial membrane and infrapatellar fat pad and plasma levels of the cytokines studied. In addition, RA patients showed a statistically significant negative correlation between AdipoR1 expression in the synovial membrane and plasma levels of TNF-α, IL-7, IL-12 and IL-13, and a significant negative correlation between AdipoR1 expression in the infrapatellar fat pad and plasma levels of IL-1β.</p></div><div><h3>Conclusions</h3><p>Adiponectin and its receptors showed the correlations with several plasma cytokines, however, a thorough understanding of the role of adiponectin in RA and OA requires further investigation.</p></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"172 ","pages":"Article 106824"},"PeriodicalIF":2.9,"publicationDate":"2024-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140028880","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":"Biochemical evaluation of possible protective effect of purslane extract in experimentally induced arthritis associated with obesity","authors":"Mohamed G. Elharrif ,&nbsp;H.A. Abdel Maksoud ,&nbsp;M.H. Abdullah ,&nbsp;Alaa S. Abd Elmohsen","doi":"10.1016/j.prostaglandins.2024.106823","DOIUrl":"10.1016/j.prostaglandins.2024.106823","url":null,"abstract":"<div><p>Arthritis, a prevalent inflammatory condition, is often linked to obesity as a contributing factor. This study aimed to assess the potential protective effects of purslane extract in male albino rats with induced arthritis and obesity. Fifty rats were randomly assigned to five groups: a control group, an induced arthritis-high-fat diet group, a high-dose purslane extract-supplemented group (300 mg/kg body weight) for 8 weeks, a low-dose purslane extract-supplemented group (150 mg/kg body weight) for 8 weeks, and a metformin-supplemented group. Arthritis was induced in the rats using Complete Freund’s Adjuvant. Plasma biomarkers, including Total Cholesterol, Triglycerides, HDL-cholesterol, LDL-cholesterol, C Reactive Protein (CRP), Erythrocyte Sedimentation Rate (ESR), Rheumatoid Factor (RF), and Anti-CCP, were assessed in each group. The results revealed a significant improvement in these biomarkers in the high-dose purslane-supplemented group (300 mg/kg body weight) compared to the induced arthritis-high-fat-diet group. This suggests a potential protective role of purslane against arthritis associated with obesity, likely attributed to its lipolytic capacity and anti-inflammatory properties. These findings contribute to our understanding of the interplay between obesity, arthritis, and natural interventions, providing valuable insights for future therapeutic approaches.</p></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"172 ","pages":"Article 106823"},"PeriodicalIF":2.9,"publicationDate":"2024-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139973268","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":"High-fat and carbohydrate diet caused chronic kidney damage by disrupting kidney function, caspase-3, oxidative stress and inflammation","authors":"Zeynep Erdemli ,&nbsp;Mehmet Gul ,&nbsp;Elif Kayhan ,&nbsp;Nurcan Gokturk ,&nbsp;Harika Gozukara Bag ,&nbsp;Mehmet Erman Erdemli","doi":"10.1016/j.prostaglandins.2024.106822","DOIUrl":"10.1016/j.prostaglandins.2024.106822","url":null,"abstract":"<div><p>The study aimed to compare the effects of a diet rich in fat, carbohydrates and protein on rat kidneys. The study was conducted on 40 <em>Wistar albino</em> rats bred at İnönü University Faculty of Medicine after the approval of the ethics committee. Rats were randomly divided into 4 groups: Control group, and the groups where the animals were fed with high carbohydrate, fat and protein rich feed. After the applications, the rat kidney tissues were removed by laparoscopy under anesthesia and blood samples were collected. 13 weeks long fat-rich and carbohydrate feed application had negative effects on oxidant-antioxidant balance, oxidative stress index, inflammation markers, kidney functions tests, histopathology and immunohistochemistry caspase-3 findings in rat kidney tissues, especially in the carbohydrate group when compared to the controls. Protein-rich feed, there were no significant difference in biochemical and histopathology compared to the control group. Fat and carbohydrate rich feed led to an increase in oxidative stress in rat kidney tissues. Oxidative stress led to nephrotoxicity, which in turn led to chronic kidney tissue damages. A more balanced and protein-rich diet instead of excessive sugar and fatty food intake could be suggested to prevent chronic kidney damage.</p></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"172 ","pages":"Article 106822"},"PeriodicalIF":2.9,"publicationDate":"2024-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139940707","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":"Sevoflurane alleviates inflammation, apoptosis and permeability damage of human umbilical vein endothelial cells induced by lipopolysaccharide by inhibiting endoplasmic reticulum stress via upregulating RORα","authors":"Weiwei Ni ,&nbsp;Zhiwei Zou ,&nbsp;Ping Jiang ,&nbsp;Shuo Wang","doi":"10.1016/j.prostaglandins.2024.106821","DOIUrl":"10.1016/j.prostaglandins.2024.106821","url":null,"abstract":"<div><p>Endothelial dysfunction often accompanies sepsis. Sevoflurane (Sev) is a widely used inhaled anesthetic that has a protective effect on sepsis-associated damage. We aimed to elucidate the role of Sev in endothelial dysfunction by using a model of LPS induced HUVECs. Sev increased the viability and decreased the apoptosis of HUVECs exposed to LPS. Inflammation and endothelial cell adhesion were improved after Sev addition. Besides, Sev alleviated LPS-induced endothelial cell permeability damage in HUVECs. RORα served as a potential protein that bound to Sev. Importantly, Sev upregulated RORα expression and inhibited endoplasmic reticulum (ER) stress in LPS-treated HUVECs. RORα silencing reversed the impacts of Sev on ER stress. Moreover, RORα deficiency or tunicamycin (ER stress inducer) treatment restored the effects of Sev on the viability, apoptosis, inflammation and endothelial permeability damage of HUVECs exposed to LPS. Taken together, Sev ameliorated LPS-induced endothelial cell damage by targeting RORα to inhibit ER stress.</p></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"172 ","pages":"Article 106821"},"PeriodicalIF":2.9,"publicationDate":"2024-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139906404","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}