title: Ischemic postconditioning alleviates neuronal injury caused by relief of carotid stenosis in a rat model of cerebral hypoperfusion.
abstract: The effects of early relief of heavy bilateral carotid stenosis and ischemic postconditioning on hippocampus CA1 neurons are still unclear. In this study, we used a rat model to imitate severe bilateral carotid stenosis in humans. The rats were divided into sham group, carotid stenosis group, stenosis relief group and ischemic postconditioning group. Ischemic postconditioning consisted of three cycles of 30 s ischemia and 30 s reperfusion. The cerebral blood flow was measured with a laser Doppler flowmeter. Neuronal death in the CA1 region was observed by hematoxylin-eosin staining, and the number of live neurons was assessed by cell counting under a light microscope. The levels of oxidative products MDA and 8-iso-PGF2α, inflammatory factors IL-1β and TNF-α, and the activities of anti-oxidative enzymes SOD and CAT were assayed by specific enzyme-linked immunosorbent assay (ELISA) kits, respectively. We found that relief of carotid stenosis and ischemic postconditioning could increase cerebral blood flow. When stenosis was relieved, the percentage of live neurons was 66.6% ± 6.2% on day 3 and 62.3% ± 9.8% on day 27, which was significantly higher than 55.5% ± 4.8% in stenosis group. Ischemic postconditioning markedly improved the live neurons to 92.5% ± 6.7% on day 3 and 88.6% ± 9.1% on day 27. Further study showed that, neuronal death caused by relief of stenosis is associated with increased oxidative stress and enhanced inflammatory response, and the protection of ischemic postconditioning is related to inhibition of oxidative stress and suppression of inflammatory response.
authors.affiliation: Department of Anesthesiology, First Bethune Hospital of Jilin University, Changchun 130021, China. pengfeige@gmail.com.
authors.forename: Chunsheng
authors.initials: C
authors.lastname: Feng
authors.forename: Tianfei
authors.initials: T
authors.lastname: Luo
authors.forename: Li
authors.initials: L
authors.lastname: Qi
authors.forename: Boyu
authors.initials: B
authors.lastname: Wang
authors.forename: Yinan
authors.initials: Y
authors.lastname: Luo
authors.forename: Pengfei
authors.initials: P
authors.lastname: Ge
mesh_terms: D000818:Animals; D017209:Apoptosis; D016893:Carotid Stenosis / Q000378:metabolism / Q000473:pathology*; D002374:Catalase / Q000032:analysis; D015237:Dinoprost / Q000031:analogs & derivatives / Q000032:analysis; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D006624:Hippocampus / Q000293:injuries / Q000378:metabolism / Q000473:pathology*; D053583:Interleukin-1beta / Q000032:analysis; D057775:Ischemic Postconditioning; D008297:Male; D008315:Malondialdehyde / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha; C075750:8-epi-prostaglandin F2alpha; D008315:Malondialdehyde; D015237:Dinoprost; D002374:Catalase; D013482:Superoxide Dismutase