Mallikarjuna R Sunkara, Jitendra N Singh, C L Meena, A B Pant, Rahul Jain, Shyam S Sharma
{"title":"一种新的促甲状腺激素释放激素(TRH)类似物PYR-l-(2,5-二溴)-His-l-ProNH2可改善谷氨酸诱导的毒性。","authors":"Mallikarjuna R Sunkara, Jitendra N Singh, C L Meena, A B Pant, Rahul Jain, Shyam S Sharma","doi":"10.1177/09727531241305505","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Glutamate has been implicated in the pathophysiology of central nervous system diseases, including stroke.</p><p><strong>Purpose: </strong>In this study, the neuroprotective potential of the newly synthesised thyrotropin-releasing hormone (TRH) analogue [Pyr-l-(2,5-dibromo)-His-l-ProNH<sub>2</sub>; NP-2376] against glutamate-induced injury model were investigated.</p><p><strong>Methods: </strong>Cortical neurons isolated from neonatal rats were used to evaluate the effects of the NP-2376. Cortical neurons were pre-treated with NP-2376 (6, 12 and 24 h) prior to glutamate (15 mM) exposure. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and neutral red uptake (NRU) assay, and oxidative stress by chloromethyl-2,7-dichlorodihydrofluorescein diacetate (DCFH-DA) and glutathione assays.</p><p><strong>Results: </strong>NP-2376 protected against glutamate-induced cortical neuron death and oxidative stress in a dose-dependent manner.</p><p><strong>Conclusions: </strong>This study demonstrates the neuroprotective potential of TRH analogue NP-2376 against glutamate-induced toxicity, which is attributed to a decrease in oxidative stress.</p>","PeriodicalId":7921,"journal":{"name":"Annals of Neurosciences","volume":" ","pages":"09727531241305505"},"PeriodicalIF":1.8000,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11907565/pdf/","citationCount":"0","resultStr":"{\"title\":\"Amelioration of Glutamate-induced Toxicity by a New Thyrotropin-releasing Hormone (TRH) Analogue PYR-l-(2,5-Dibromo)-His-l-ProNH<sub>2</sub>.\",\"authors\":\"Mallikarjuna R Sunkara, Jitendra N Singh, C L Meena, A B Pant, Rahul Jain, Shyam S Sharma\",\"doi\":\"10.1177/09727531241305505\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Glutamate has been implicated in the pathophysiology of central nervous system diseases, including stroke.</p><p><strong>Purpose: </strong>In this study, the neuroprotective potential of the newly synthesised thyrotropin-releasing hormone (TRH) analogue [Pyr-l-(2,5-dibromo)-His-l-ProNH<sub>2</sub>; NP-2376] against glutamate-induced injury model were investigated.</p><p><strong>Methods: </strong>Cortical neurons isolated from neonatal rats were used to evaluate the effects of the NP-2376. Cortical neurons were pre-treated with NP-2376 (6, 12 and 24 h) prior to glutamate (15 mM) exposure. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and neutral red uptake (NRU) assay, and oxidative stress by chloromethyl-2,7-dichlorodihydrofluorescein diacetate (DCFH-DA) and glutathione assays.</p><p><strong>Results: </strong>NP-2376 protected against glutamate-induced cortical neuron death and oxidative stress in a dose-dependent manner.</p><p><strong>Conclusions: </strong>This study demonstrates the neuroprotective potential of TRH analogue NP-2376 against glutamate-induced toxicity, which is attributed to a decrease in oxidative stress.</p>\",\"PeriodicalId\":7921,\"journal\":{\"name\":\"Annals of Neurosciences\",\"volume\":\" \",\"pages\":\"09727531241305505\"},\"PeriodicalIF\":1.8000,\"publicationDate\":\"2025-03-13\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11907565/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Annals of Neurosciences\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1177/09727531241305505\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annals of Neurosciences","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1177/09727531241305505","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
Amelioration of Glutamate-induced Toxicity by a New Thyrotropin-releasing Hormone (TRH) Analogue PYR-l-(2,5-Dibromo)-His-l-ProNH2.
Background: Glutamate has been implicated in the pathophysiology of central nervous system diseases, including stroke.
Purpose: In this study, the neuroprotective potential of the newly synthesised thyrotropin-releasing hormone (TRH) analogue [Pyr-l-(2,5-dibromo)-His-l-ProNH2; NP-2376] against glutamate-induced injury model were investigated.
Methods: Cortical neurons isolated from neonatal rats were used to evaluate the effects of the NP-2376. Cortical neurons were pre-treated with NP-2376 (6, 12 and 24 h) prior to glutamate (15 mM) exposure. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and neutral red uptake (NRU) assay, and oxidative stress by chloromethyl-2,7-dichlorodihydrofluorescein diacetate (DCFH-DA) and glutathione assays.
Results: NP-2376 protected against glutamate-induced cortical neuron death and oxidative stress in a dose-dependent manner.
Conclusions: This study demonstrates the neuroprotective potential of TRH analogue NP-2376 against glutamate-induced toxicity, which is attributed to a decrease in oxidative stress.