Effects of recombinant activated coagulation factor VII on apoptosis and expressions of Bcl-2 and Bax in rats with intracerebral hemorrhage.

Abstract:

OBJECTIVE:To investigate the effects of recombinant activated coagulation factor VII (rFVIIa) on apoptosis and the expressions of B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax) in rats with intracerebral hemorrhage (ICH). MATERIALS AND METHODS:A total of 90 8-week-old male Sprague-Dawley (SD) rats with similar weight were selected and randomly divided into normal group (n=30), ICH control group (n=30), and rFVIIa treatment group (n=30). Five days later, hematoxylin-eosin (HE) staining was applied to observe pathological changes in rat brain in three groups. Cell apoptosis in rat brain was detected at 6 h, 12 h, 24 h, 48 h, 72 h, and 120 h, respectively. The relative expression levels of Bcl-2 and Bax in brain tissues were measured via fluorescence quantitative Polymerase Chain Reaction (qPCR) and Western blotting, respectively. RESULTS:Compared with those in ICH control group, rats in rFVIIa treatment group had fewer degenerated and necrotic nerve cells and milder pathological changes in the marginal zone. The number of apoptotic cells in ICH control group and rFVIIa group was gradually increased in a time-dependent manner, and achieved the peak at 72 h. The number of apoptotic cells in treatment group was significantly lower than that in ICH control group after 24 h (p<0.05). Both fluorescence qPCR and Western blotting results proved that in comparison with ICH control group, rFVIIa group had a higher relative expression level of Bcl-2 (p<0.05) and a lower expression level of Bax (p<0.05). CONCLUSIONS:Apoptosis mechanism may be involved in secondary brain injury after ICH. RFVIIa may have an important protective effect on neuronal injury after ICH by promoting the expression of Bcl-2 and inhibiting the expression of Bax protein.

authors

Ma YM,Zheng JX,Xu X,Shan YS,Gao ZW,Chen WG

doi

10.26355/eurrev_201808_15725

subject

Has Abstract

pub_date

2018-08-01 00:00:00

pages

5264-5269

issue

16

eissn

1128-3602

issn

2284-0729

journal_volume

22

pub_type

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