title: Improved neuronal survival of focal ischemia after delipid extracorporeal lipoprotein treatment in hyperlipidemic rabbits.
abstract: A delipid extracorporeal lipoprotein filter (DELP) system has been used to treat patients with stroke and has shown favorable prognosis. However, the mechanism for the neuronal functional recovery remains unclear. This study aimed to investigate the neuronal histological assessment, and the levels of C-reactive protein (CRP), tumor necrosis factor alpha (TNF-α), and oxidized low-density lipoprotein (oxLDL) after ischemic stroke following DELP treatment. Hyperlipidemic rabbits underwent middle cerebral artery occlusion. After 30 min, the animals received an extracorporeal apheresis treatment with a DELP filter. Total cholesterol (TC), triglyceride, and low-density lipoprotein (LDL) of the plasma were measured. The levels of CRP, TNF-α, and oxLDL in brain tissue were also measured by enzyme-linked immunosorbent assay. Hematoxylin and eosin staining, cresyl violet staining, neuron-specific enolase (NSE) and glial fibrillary acidic protein immunohistochemistry, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay were performed. DELP apheresis reduced TC and LDL by >30%. The number of neurons at day 7 (P < 0.01) and the integrated optical density of NSE at day 1 (P < 0.05) and day 7 (P < 0.01) were significantly increased in the DELP group. TUNEL-positive cells were significantly decreased (P < 0.05). Astrocytes were moderately activated, and this activation persisted up to 7 days. Gliosis was not found in the DELP group. After treatment, the level of CRP declined at day 1 (P < 0.05); TNF-α and oxLDL declined at day 7 (P < 0.05). DELP apheresis decreased neuronal apoptosis, reduced inflammatory markers and oxidative stress in cerebral ischemia, and improved neuronal survival.
authors.affiliation: Medical School of Nankai University, Tianjin, China.
authors.forename: Guojing
authors.initials: G
authors.lastname: Liu
authors.forename: Weichao
authors.initials: W
authors.lastname: Wang
authors.forename: Hui
authors.initials: H
authors.lastname: Xie
authors.forename: Yongzhe
authors.initials: Y
authors.lastname: Che
authors.forename: Jun
authors.initials: J
authors.lastname: Xue
authors.forename: Youzhen
authors.initials: Y
authors.lastname: Wu
authors.forename: Qingwen
authors.initials: Q
authors.lastname: Zhou
authors.forename: Deling
authors.initials: D
authors.lastname: Kong
mesh_terms: D000818:Animals; D001781:Blood Component Removal / Q000295:instrumentation*; D001921:Brain / Q000378:metabolism / Q000473:pathology; D002545:Brain Ischemia / Q000097:blood / Q000378:metabolism* / Q000473:pathology / Q000628:therapy*; D002097:C-Reactive Protein / Q000378:metabolism; D002470:Cell Survival; D002784:Cholesterol / Q000097:blood; D004867:Equipment Design; D006949:Hyperlipidemias / Q000097:blood / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D008074:Lipoproteins / Q000097:blood / Q000302:isolation & purification* / Q000378:metabolism; D008077:Lipoproteins, LDL / Q000097:blood / Q000302:isolation & purification / Q000378:metabolism; D008297:Male; D009474:Neurons / Q000166:cytology / Q000378:metabolism / Q000473:pathology*; D011817:Rabbits; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D008074:Lipoproteins; D008077:Lipoproteins, LDL; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; C099252:oxidized low density lipoprotein; D002097:C-Reactive Protein; D002784:Cholesterol