{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yu Y"],"funding":["National Natural Science Foundation of China"],"pagination":["1907-1922"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8525958"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["20(18)"],"pubmed_abstract":["Background Ketamine-related cystitis (KC) has been researched in many clinical studies, but its exact mechanism is ambiguous and needs further research. Methods We established a KC rat model and analyzed physiological, biochemical, and urodynamic parameters of ketamine (KET)-related bladder injury. Bladder histologic feature, reactive oxygen species (ROS), autophagy-, apoptosis-, and endoplasmic reticulum stress (ERS)-related markers were examined by hematoxylin and eosin staining, Masson staining, ROS kit, quantitative real-time polymerase chain reaction, and western blot. <i>In vitro</i>, effects of 0.01, 0.1, and 1 mM KET on cell vitality, apoptosis, ROS level, autophagy-, apoptosis-, and ERS-related markers were examined again. Effects of KET-1 and salubrinal on complex formation, auto"],"journal":["Cell cycle (Georgetown, Tex.)"],"pubmed_title":["Ketamine enhances autophagy and endoplasmic reticulum stress in rats and SV-HUC-1 cells via activating IRE1-TRAF2-ASK1-JNK pathway."],"pmcid":["PMC8525958"],"funding_grant_id":["Grant Number 81970659","Grant Number 81700664"],"pubmed_authors":["Li Y","Qiao H","Shan Z","Wu D","Yu Y"],"additional_accession":[]},"is_claimable":false,"name":"Ketamine enhances autophagy and endoplasmic reticulum stress in rats and SV-HUC-1 cells via activating IRE1-TRAF2-ASK1-JNK pathway.","description":"Background Ketamine-related cystitis (KC) has been researched in many clinical studies, but its exact mechanism is ambiguous and needs further research. Methods We established a KC rat model and analyzed physiological, biochemical, and urodynamic parameters of ketamine (KET)-related bladder injury. Bladder histologic feature, reactive oxygen species (ROS), autophagy-, apoptosis-, and endoplasmic reticulum stress (ERS)-related markers were examined by hematoxylin and eosin staining, Masson staining, ROS kit, quantitative real-time polymerase chain reaction, and western blot. <i>In vitro</i>, effects of 0.01, 0.1, and 1 mM KET on cell vitality, apoptosis, ROS level, autophagy-, apoptosis-, and ERS-related markers were examined again. Effects of KET-1 and salubrinal on complex formation, auto","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Sep","modification":"2025-04-05T14:05:18.799Z","creation":"2025-04-05T14:05:18.799Z"},"accession":"S-EPMC8525958","cross_references":{"pubmed":["34427546"],"doi":["10.1080/15384101.2021.1966199"]}}