Abstract | BACKGROUND: METHODS: Male New Zealand white rabbits were randomly subdivided into the sham-operated (SH) group, CDC group, and RDC group. Blood plasma samples and brain tissue were collected 2 days before operation (baseline) and at 3, 6, 24, and 72 hours after operation to measure the levels of UCH-L1, GFAP, oxidative stress indicators, and inflammatory cytokines by performing ELISA or Western blot. The neurological score of the rabbits and brain water content was graded 24 h after surgery. qPCR, immunofluorescence, and FJ-C staining were conducted. RESULTS: CDC improved neurological function, lowered brain water content, ameliorated neuronal degeneration, attenuated oxidative damage, and inflammatory responses to a greater extent than RDC. Plasma UCH-L1 level was significantly lower in the CDC group at 3 h postoperatively than in the RDC group. CDC reduced plasma GFAP levels to various degrees at 3 h, 6 h, and 24 h postoperatively compared with RDC. Immunofluorescence confirmed that the expression of UCH-L1 and GFAP in the cortex of the CDC group was lower than that of the RDC group. CONCLUSIONS: Our data collectively demonstrate that CDC could attenuate oxidative damage and inflammatory responses, downregulate UCH-L1 and GFAP levels, and contribute to an improved neuroprotective effect compared with RDC.
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Authors | Chonghui Zhang, Xiao Qian, Jie Zheng, Pu Ai, Xinyi Cao, Xiaofei Pan, Tao Chen, Yuhai Wang |
Journal | BioMed research international
(Biomed Res Int)
Vol. 2022
Pg. 1936691
( 2022)
ISSN: 2314-6141 [Electronic] United States |
PMID | 35187159
(Publication Type: Journal Article)
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Copyright | Copyright © 2022 Chonghui Zhang et al. |
Chemical References |
- Glial Fibrillary Acidic Protein
- Ubiquitin Thiolesterase
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Topics |
- Animals
- Decompression
(methods)
- Disease Models, Animal
- Down-Regulation
- Glial Fibrillary Acidic Protein
(metabolism)
- Intracranial Hypertension
(prevention & control)
- Male
- Neuroinflammatory Diseases
(prevention & control)
- Oxidative Stress
- Rabbits
- Ubiquitin Thiolesterase
(metabolism)
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