13 August 2016 : Original article
Effect of Urinary Kallidinogenase on Transforming Growth Factor-β1 and High-Sensitivity C-Reactive Protein Expression in Rat Focal Cerebral Ischemic Injury
Ting-Fang DongBE, Hai-Xia LvBD, Xiao-Lu NiuDF, Yong-Kun GuiCEG, Ping ZhangAEG, Hai-Qing YanBF, Tong LiDFDOI: 10.12659/MSM.892724
Med Sci Monit 2016; 22:2852-2858
Abstract
BACKGROUND: In this study we investigated the effect of urinary kallidinogenase (UK) on transforming growth factor beta 1 (TGF-β1) 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 AND 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-β1 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-β1 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-β1 expression and inhibiting excessive inflammatory responses.
Keywords: Brain Ischemia - urine, C-Reactive Protein - biosynthesis, Kallikreins - urine, Reperfusion Injury - metabolism, Transforming Growth Factor beta1 - biosynthesis
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