{"title":"MiR-145-5p靶向成纤维细胞生长因子-5参与神经元缺血再灌注损伤","authors":"Lei Xu","doi":"10.31901/24566330.2024/24.01.809","DOIUrl":null,"url":null,"abstract":"The researchers made efforts in elucidating the mechanism for miR-145-5p participating in neuronal ischemia/reperfusion injury (I/R) via targeting fibroblast growth factor-5 (FGF5). OGD/R was performed to construct the neuronal injury model. After OGD/R, the oxidative stress injury of nerve cells was enhanced significantly, the levels of lactic dehydrogenase, reactive oxygen species and malondialdehyde rose, while the superoxide dismutase activity decreased. Both miR-145-5p and cell apoptosis rate increased. MiR-145-5p had a targeting relation to FGF5. After miR- 145-5p inhibitor transfection of nerve cells, inhibition of oxidative stress together with apoptosis was observed. FGF5 siRNA could reverse the impact on oxidative stress, FGF5, and apoptosis exerted by miR-145-5p-inhibitor in the OGD/ R model. Being a latent target of I/R treatment, miR-145-5p induces the oxidative stress injury as well as apoptosis of HT22 cells by targeting and binding FGF5.","PeriodicalId":54956,"journal":{"name":"International Journal of Human Genetics","volume":"6 1","pages":"0"},"PeriodicalIF":0.1000,"publicationDate":"2023-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Participation of MiR-145-5p in Neuronal Ischemia/Reperfusion Injury by Targeting Fibroblast Growth Factor-5\",\"authors\":\"Lei Xu\",\"doi\":\"10.31901/24566330.2024/24.01.809\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"The researchers made efforts in elucidating the mechanism for miR-145-5p participating in neuronal ischemia/reperfusion injury (I/R) via targeting fibroblast growth factor-5 (FGF5). OGD/R was performed to construct the neuronal injury model. After OGD/R, the oxidative stress injury of nerve cells was enhanced significantly, the levels of lactic dehydrogenase, reactive oxygen species and malondialdehyde rose, while the superoxide dismutase activity decreased. Both miR-145-5p and cell apoptosis rate increased. MiR-145-5p had a targeting relation to FGF5. After miR- 145-5p inhibitor transfection of nerve cells, inhibition of oxidative stress together with apoptosis was observed. FGF5 siRNA could reverse the impact on oxidative stress, FGF5, and apoptosis exerted by miR-145-5p-inhibitor in the OGD/ R model. Being a latent target of I/R treatment, miR-145-5p induces the oxidative stress injury as well as apoptosis of HT22 cells by targeting and binding FGF5.\",\"PeriodicalId\":54956,\"journal\":{\"name\":\"International Journal of Human Genetics\",\"volume\":\"6 1\",\"pages\":\"0\"},\"PeriodicalIF\":0.1000,\"publicationDate\":\"2023-10-17\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International Journal of Human Genetics\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.31901/24566330.2024/24.01.809\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"GENETICS & HEREDITY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Human Genetics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.31901/24566330.2024/24.01.809","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}
Participation of MiR-145-5p in Neuronal Ischemia/Reperfusion Injury by Targeting Fibroblast Growth Factor-5
The researchers made efforts in elucidating the mechanism for miR-145-5p participating in neuronal ischemia/reperfusion injury (I/R) via targeting fibroblast growth factor-5 (FGF5). OGD/R was performed to construct the neuronal injury model. After OGD/R, the oxidative stress injury of nerve cells was enhanced significantly, the levels of lactic dehydrogenase, reactive oxygen species and malondialdehyde rose, while the superoxide dismutase activity decreased. Both miR-145-5p and cell apoptosis rate increased. MiR-145-5p had a targeting relation to FGF5. After miR- 145-5p inhibitor transfection of nerve cells, inhibition of oxidative stress together with apoptosis was observed. FGF5 siRNA could reverse the impact on oxidative stress, FGF5, and apoptosis exerted by miR-145-5p-inhibitor in the OGD/ R model. Being a latent target of I/R treatment, miR-145-5p induces the oxidative stress injury as well as apoptosis of HT22 cells by targeting and binding FGF5.