{"title":"NLPR3炎性小体增加神经炎症加速抑郁样行为","authors":"Jie Liu, Enyan Yu","doi":"10.2174/1567202619666220829110111","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Depression is a class of important mental illness, which has become a severe health problem perplexing the world due to its high morbidity rate, high disability rate, and great disease burden. This study aimed to evaluate the role and possible mechanisms of P2RY12 in the depression-like behaviors model.</p><p><strong>Methods: </strong>Serum samples of patients with depression-like behaviors were used to analyze the expression of P2RY12. Models of mice were given LPS via intraperitoneal injection for 7 days. Behavioral tests were executed in this experiment.</p><p><strong>Results: </strong>The expression of P2RY12 in models of depression-like behaviors or mice with depression- like behaviors were induced. The inhibition of P2RY12 presents depression-like behaviors and reduces inflammation in the model of depression-like behaviors. P2RY12 induced NLRP3 expression and suppressed NLRP3 ubiquitination in a model of depression-like behavior. The inhibition of NLRP3 reduced the effects of P2RY12 in mice model of depression-like behaviors. The regulation of NLRP3 controlled the effects of the P2RY12 in vitro model of depression-like behaviors.</p><p><strong>Conclusion: </strong>We conclude that P2RY12 increased neuroinflammation to accelerate depression-like behaviors by NLPR3 inflammasome, providing novel information for the treatment of depressionlike behaviors.</p>","PeriodicalId":10879,"journal":{"name":"Current neurovascular research","volume":"19 3","pages":"267-274"},"PeriodicalIF":2.0000,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"P2RY12 Increased Neuroinflammation to Accelerate Depression-like Behaviors by the NLPR3 Inflammasome.\",\"authors\":\"Jie Liu, Enyan Yu\",\"doi\":\"10.2174/1567202619666220829110111\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>Depression is a class of important mental illness, which has become a severe health problem perplexing the world due to its high morbidity rate, high disability rate, and great disease burden. This study aimed to evaluate the role and possible mechanisms of P2RY12 in the depression-like behaviors model.</p><p><strong>Methods: </strong>Serum samples of patients with depression-like behaviors were used to analyze the expression of P2RY12. Models of mice were given LPS via intraperitoneal injection for 7 days. Behavioral tests were executed in this experiment.</p><p><strong>Results: </strong>The expression of P2RY12 in models of depression-like behaviors or mice with depression- like behaviors were induced. The inhibition of P2RY12 presents depression-like behaviors and reduces inflammation in the model of depression-like behaviors. P2RY12 induced NLRP3 expression and suppressed NLRP3 ubiquitination in a model of depression-like behavior. The inhibition of NLRP3 reduced the effects of P2RY12 in mice model of depression-like behaviors. The regulation of NLRP3 controlled the effects of the P2RY12 in vitro model of depression-like behaviors.</p><p><strong>Conclusion: </strong>We conclude that P2RY12 increased neuroinflammation to accelerate depression-like behaviors by NLPR3 inflammasome, providing novel information for the treatment of depressionlike behaviors.</p>\",\"PeriodicalId\":10879,\"journal\":{\"name\":\"Current neurovascular research\",\"volume\":\"19 3\",\"pages\":\"267-274\"},\"PeriodicalIF\":2.0000,\"publicationDate\":\"2022-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Current neurovascular research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.2174/1567202619666220829110111\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"CLINICAL NEUROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current neurovascular research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.2174/1567202619666220829110111","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
P2RY12 Increased Neuroinflammation to Accelerate Depression-like Behaviors by the NLPR3 Inflammasome.
Introduction: Depression is a class of important mental illness, which has become a severe health problem perplexing the world due to its high morbidity rate, high disability rate, and great disease burden. This study aimed to evaluate the role and possible mechanisms of P2RY12 in the depression-like behaviors model.
Methods: Serum samples of patients with depression-like behaviors were used to analyze the expression of P2RY12. Models of mice were given LPS via intraperitoneal injection for 7 days. Behavioral tests were executed in this experiment.
Results: The expression of P2RY12 in models of depression-like behaviors or mice with depression- like behaviors were induced. The inhibition of P2RY12 presents depression-like behaviors and reduces inflammation in the model of depression-like behaviors. P2RY12 induced NLRP3 expression and suppressed NLRP3 ubiquitination in a model of depression-like behavior. The inhibition of NLRP3 reduced the effects of P2RY12 in mice model of depression-like behaviors. The regulation of NLRP3 controlled the effects of the P2RY12 in vitro model of depression-like behaviors.
Conclusion: We conclude that P2RY12 increased neuroinflammation to accelerate depression-like behaviors by NLPR3 inflammasome, providing novel information for the treatment of depressionlike behaviors.
期刊介绍:
Current Neurovascular Research provides a cross platform for the publication of scientifically rigorous research that addresses disease mechanisms of both neuronal and vascular origins in neuroscience. The journal serves as an international forum publishing novel and original work as well as timely neuroscience research articles, full-length/mini reviews in the disciplines of cell developmental disorders, plasticity, and degeneration that bridges the gap between basic science research and clinical discovery. Current Neurovascular Research emphasizes the elucidation of disease mechanisms, both cellular and molecular, which can impact the development of unique therapeutic strategies for neuronal and vascular disorders.