Tayyaba Tahir, Qurat-Ul-Ain, Ammara Saleem, Shahnaz, Muhammad Imran Khan, Kanwal Akhtar, Irfan Hamid, Rabia Iqbal, Zulcaif Ahmad, Muhammad Furqan Akhtar
{"title":"四氢嘧啶衍生物通过调节氧化和炎症标志物显示对氯胺酮诱导的精神分裂症的神经保护作用。","authors":"Tayyaba Tahir, Qurat-Ul-Ain, Ammara Saleem, Shahnaz, Muhammad Imran Khan, Kanwal Akhtar, Irfan Hamid, Rabia Iqbal, Zulcaif Ahmad, Muhammad Furqan Akhtar","doi":"10.1007/s11011-025-01651-5","DOIUrl":null,"url":null,"abstract":"<p><p>Schizophrenia impacts individuals' cognition, perceptions, behavior and memory and influences almost 1-1.5% of the global population. It is a psychotic disorder possibly caused by high levels of immunostimulants as well as oxygen-derived free radicals in the blood and CSF. As observed in the studies that pyrimidine derivatives (THP) have promising potential to act as anti-inflammatory agents, therefore these may be helpful in treating schizophrenia. So, this study evaluated the preventive potential of THP in treating schizophrenia induced by ketamine. The mice were segregated in six groups, normal control received 0.5% CMC 1 ml/kg I.P.), disease control and other groups received ketamine 10 mg/kg I.P. Clozapine (1 mg/kg I.P.) served as standard drug. Other groups received THP (10 mg/kg/day I.P.), THP (15 mg/kg/day I.P.) and THP (20 mg/kg/day I.P.). Study was designed as a preventive trial spanning 21-days with initial 14 days treatment, followed by a subsequent 7-day ketamine administration. The study demonstrated that the improvement of positive, negative and cognitive symptoms in THP-treated animals by significantly reducing stereotypic behaviors and inactivity in forced swim and tail suspension tests, and accelerating center time in Open field test and number of entries and alteration in Y-maze test. Oxidative stress in schizophrenic mice was also managed by marked elevation in SOD and CAT levels, and the parameters like GSH, MDA and nitrite contents were significantly reduced. In addition, inflammatory markers such as TNF-α, IL-6, NF-κB and MAP-K were significantly reduced. Furthermore, gene expression showed significant incline in BDNF levels, after THP administration in schizophrenic mice. Overall, the study disclosed THP as an effective compound in mitigating the symptoms of schizophrenia, however further study is needed to evaluate its toxicity profile.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 6","pages":"247"},"PeriodicalIF":3.5000,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"A tetrahydropyrimidine derivative demonstrates neuroprotection against ketamine-induced schizophrenia through moderating oxidative and inflammatory markers.\",\"authors\":\"Tayyaba Tahir, Qurat-Ul-Ain, Ammara Saleem, Shahnaz, Muhammad Imran Khan, Kanwal Akhtar, Irfan Hamid, Rabia Iqbal, Zulcaif Ahmad, Muhammad Furqan Akhtar\",\"doi\":\"10.1007/s11011-025-01651-5\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Schizophrenia impacts individuals' cognition, perceptions, behavior and memory and influences almost 1-1.5% of the global population. It is a psychotic disorder possibly caused by high levels of immunostimulants as well as oxygen-derived free radicals in the blood and CSF. As observed in the studies that pyrimidine derivatives (THP) have promising potential to act as anti-inflammatory agents, therefore these may be helpful in treating schizophrenia. So, this study evaluated the preventive potential of THP in treating schizophrenia induced by ketamine. The mice were segregated in six groups, normal control received 0.5% CMC 1 ml/kg I.P.), disease control and other groups received ketamine 10 mg/kg I.P. Clozapine (1 mg/kg I.P.) served as standard drug. Other groups received THP (10 mg/kg/day I.P.), THP (15 mg/kg/day I.P.) and THP (20 mg/kg/day I.P.). Study was designed as a preventive trial spanning 21-days with initial 14 days treatment, followed by a subsequent 7-day ketamine administration. The study demonstrated that the improvement of positive, negative and cognitive symptoms in THP-treated animals by significantly reducing stereotypic behaviors and inactivity in forced swim and tail suspension tests, and accelerating center time in Open field test and number of entries and alteration in Y-maze test. Oxidative stress in schizophrenic mice was also managed by marked elevation in SOD and CAT levels, and the parameters like GSH, MDA and nitrite contents were significantly reduced. In addition, inflammatory markers such as TNF-α, IL-6, NF-κB and MAP-K were significantly reduced. Furthermore, gene expression showed significant incline in BDNF levels, after THP administration in schizophrenic mice. Overall, the study disclosed THP as an effective compound in mitigating the symptoms of schizophrenia, however further study is needed to evaluate its toxicity profile.</p>\",\"PeriodicalId\":18685,\"journal\":{\"name\":\"Metabolic brain disease\",\"volume\":\"40 6\",\"pages\":\"247\"},\"PeriodicalIF\":3.5000,\"publicationDate\":\"2025-08-14\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Metabolic brain disease\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s11011-025-01651-5\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"ENDOCRINOLOGY & METABOLISM\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Metabolic brain disease","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s11011-025-01651-5","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
A tetrahydropyrimidine derivative demonstrates neuroprotection against ketamine-induced schizophrenia through moderating oxidative and inflammatory markers.
Schizophrenia impacts individuals' cognition, perceptions, behavior and memory and influences almost 1-1.5% of the global population. It is a psychotic disorder possibly caused by high levels of immunostimulants as well as oxygen-derived free radicals in the blood and CSF. As observed in the studies that pyrimidine derivatives (THP) have promising potential to act as anti-inflammatory agents, therefore these may be helpful in treating schizophrenia. So, this study evaluated the preventive potential of THP in treating schizophrenia induced by ketamine. The mice were segregated in six groups, normal control received 0.5% CMC 1 ml/kg I.P.), disease control and other groups received ketamine 10 mg/kg I.P. Clozapine (1 mg/kg I.P.) served as standard drug. Other groups received THP (10 mg/kg/day I.P.), THP (15 mg/kg/day I.P.) and THP (20 mg/kg/day I.P.). Study was designed as a preventive trial spanning 21-days with initial 14 days treatment, followed by a subsequent 7-day ketamine administration. The study demonstrated that the improvement of positive, negative and cognitive symptoms in THP-treated animals by significantly reducing stereotypic behaviors and inactivity in forced swim and tail suspension tests, and accelerating center time in Open field test and number of entries and alteration in Y-maze test. Oxidative stress in schizophrenic mice was also managed by marked elevation in SOD and CAT levels, and the parameters like GSH, MDA and nitrite contents were significantly reduced. In addition, inflammatory markers such as TNF-α, IL-6, NF-κB and MAP-K were significantly reduced. Furthermore, gene expression showed significant incline in BDNF levels, after THP administration in schizophrenic mice. Overall, the study disclosed THP as an effective compound in mitigating the symptoms of schizophrenia, however further study is needed to evaluate its toxicity profile.
期刊介绍:
Metabolic Brain Disease serves as a forum for the publication of outstanding basic and clinical papers on all metabolic brain disease, including both human and animal studies. The journal publishes papers on the fundamental pathogenesis of these disorders and on related experimental and clinical techniques and methodologies. Metabolic Brain Disease is directed to physicians, neuroscientists, internists, psychiatrists, neurologists, pathologists, and others involved in the research and treatment of a broad range of metabolic brain disorders.