Effects of vinpocetine on inflammation of brain in rats with intracerebral hemorrhage
10.3969/j.issn.1000-4718.2017.12.005
- VernacularTitle:长春西汀减轻脑出血大鼠脑组织的炎症损伤
- Author:
ping Jian SUN
1
;
ping Fu LI
;
juan Zhao XU
;
ying Jian BAI
;
xia Jiang YANG
;
fen Xiu ZHANG
;
qing Cui LI
;
Dong ZHAO
Author Information
1. 河北医科大学第二医院神经外科
- Keywords:
Vinpocetine;
Intracerebral hemorrhage;
Toll-like receptors 4;
Nuclear factor-κB;
Adhesion mole-cules
- From:
Chinese Journal of Pathophysiology
2017;33(12):2139-2142
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the effects of vinpocetine on inflammation of brain in intracerebral hemorrhage ( ICH) rats and to explore the underlying mechanisms .METHODS:All rats were randomly divided into sham group , ICH group, ICH with low dose of vinpocetine treatment group , ICH with medium dose of vinpocetine treatment group , and ICH with high dose of vinpocetine treatment group .Except sham group , the rats in other groups were injected with type VII col-lagenase to establish ICH model , and then the rats in vinpocetine treatment groups were received vinpocetine at 0.5, 1.0 or 1.5 mg/kg by intraperitoneal injection once a day for 7 days.After corresponding treatment , the impairment of neurological function in the rats was scored and the water content of the brain tissues was measured .Moreover, the activity of myeloper-oxidase (MPO) was determined by ELISA, and the protein expression of Toll-like receptors 4 (TLR4), nuclear factor-κB (NF-κB), intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molcule-1 (VCAM-1) in the brain tissues was determined by Western blot .RESULTS: Compared with ICH group , vinpocetine treatment significantly de-creased the scores of the impairment of neurological function and the water content of the brain tissues .Moreover, the activ-ity of MPO and the protein expression of TLR4, NF-κB, ICAM-1 and VCAM-1 were also reduced after vinpocetine treat-ment (P<0.05).CONCLUSION:Vinpocetine improves neurological function in ICH rats via suppression of inflamma -tion by inhibiting NF-κB signaling and expression of ICAM-1 and VCAM-1.
