{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["13"],"submitter":["Gao Q"],"pubmed_abstract":["The beneficial properties of Sodium Danshensu (SDSS) for controlling cerebral ischemia and reperfusion injury (CIRI) are elucidated here both <i>in vivo</i> and <i>in vitro</i>. SDSS administration significantly improved the viability of P12 cells, reduced lactate dehydrogenase (LDH) leakage, and decreased the apoptosis rate following exposure to an oxygen-glucose deprivation/reoxygenation (OGD) environment. In addition, the results of a Huprot<sup>TM</sup> human protein microarray and network pharmacology indicated that AKT1 is one of the main targets of SDSS. Moreover, functional experiments showed that SDSS intervention markedly increased the phosphorylation level of AKT1 and its downstream regulator, mTOR. The binding sites of SDSS to AKT1 protein were confirmed by Autodock software an"],"journal":["Frontiers in pharmacology"],"pagination":["946668"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9520076"],"repository":["biostudies-literature"],"pubmed_title":["Sodium danshensu attenuates cerebral ischemia-reperfusion injury by targeting AKT1."],"pmcid":["PMC9520076"],"pubmed_authors":["Gao Q","Guo M","Yang Z","Yu B","Zhang Y","Zeng M","Jiang X","Yang Q","Yuan X","Zeng W","Deng H"],"additional_accession":[]},"is_claimable":false,"name":"Sodium danshensu attenuates cerebral ischemia-reperfusion injury by targeting AKT1.","description":"The beneficial properties of Sodium Danshensu (SDSS) for controlling cerebral ischemia and reperfusion injury (CIRI) are elucidated here both <i>in vivo</i> and <i>in vitro</i>. SDSS administration significantly improved the viability of P12 cells, reduced lactate dehydrogenase (LDH) leakage, and decreased the apoptosis rate following exposure to an oxygen-glucose deprivation/reoxygenation (OGD) environment. In addition, the results of a Huprot<sup>TM</sup> human protein microarray and network pharmacology indicated that AKT1 is one of the main targets of SDSS. Moreover, functional experiments showed that SDSS intervention markedly increased the phosphorylation level of AKT1 and its downstream regulator, mTOR. The binding sites of SDSS to AKT1 protein were confirmed by Autodock software an","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022","modification":"2026-05-27T19:12:24.227Z","creation":"2025-05-18T12:49:01.953Z"},"accession":"S-EPMC9520076","cross_references":{"pubmed":["36188542"],"doi":["10.3389/fphar.2022.946668"]}}