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Effect of Urinary Kallidinogenase on Transforming Growth Factor-β(1) and High-Sensitivity C-Reactive Protein Expression in Rat Focal Cerebral Ischemic Injury
BACKGROUND: In this study we investigated the effect of urinary kallidinogenase (UK) on transforming growth factor beta 1 (TGF-β(1)) expression in brain tissue. We also explored the neuroprotective mechanism of UK against ischemic injury by measuring serum high-sensitivity C-reactive protein (hs-CRP...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scientific Literature, Inc.
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4988362/ https://www.ncbi.nlm.nih.gov/pubmed/27521289 http://dx.doi.org/10.12659/MSM.892724 |
Sumario: | BACKGROUND: In this study we investigated the effect of urinary kallidinogenase (UK) on transforming growth factor beta 1 (TGF-β(1)) expression in brain tissue. We also explored the neuroprotective mechanism of UK against ischemic injury by measuring serum high-sensitivity C-reactive protein (hs-CRP) level changes after rat cerebral ischemic injury. MATERIAL/METHODS: The rat middle cerebral artery ischemia/reperfusion model was established using the suture method. Sprague-Dawley rats were randomly divided into 3 groups: treatment, Gegen control, and blank control. Each group was subsequently divided into 5 subgroups according to time (6, 12, 24, 48, and 72 h). Rats in the treatment group were administered UK as treatment. TGF-β(1) expression was observed at each time point using SABC and immunohistochemical staining methods to estimate cerebral infarct volume percentage. Serum hs-CRP levels were also measured. RESULTS: TGF-β(1) protein expression in ischemic brain tissues of the treatment group significantly increased at each time point (P<0.01) compared with both control groups. Treatment group serum hs-CRP levels significantly decreased at each time point (P<0.05) compared with both control groups. CONCLUSIONS: UK exerts a neuroprotective effect by upregulating TGF-β(1) expression and inhibiting excessive inflammatory responses. |
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