{"title":"通过阻断 MAPK/NF-κB 信号通路抑制内质网应激,沉默 PDCD4 可减轻 KA 诱导的 HT22 细胞神经毒性","authors":"Peng Li, Guiling Cao","doi":"10.3892/etm.2023.12343","DOIUrl":null,"url":null,"abstract":"","PeriodicalId":12285,"journal":{"name":"Experimental and therapeutic medicine","volume":"45 10","pages":""},"PeriodicalIF":2.4000,"publicationDate":"2023-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"PDCD4 silencing alleviates KA‑induced neurotoxicity of HT22 cells by inhibiting endoplasmic reticulum stress via blocking the MAPK/NF‑κB signaling pathway\",\"authors\":\"Peng Li, Guiling Cao\",\"doi\":\"10.3892/etm.2023.12343\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"\",\"PeriodicalId\":12285,\"journal\":{\"name\":\"Experimental and therapeutic medicine\",\"volume\":\"45 10\",\"pages\":\"\"},\"PeriodicalIF\":2.4000,\"publicationDate\":\"2023-12-06\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Experimental and therapeutic medicine\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.3892/etm.2023.12343\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experimental and therapeutic medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3892/etm.2023.12343","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
PDCD4 silencing alleviates KA‑induced neurotoxicity of HT22 cells by inhibiting endoplasmic reticulum stress via blocking the MAPK/NF‑κB signaling pathway