Ischemic postconditioning inhibited the proliferation of astrocyte following cerebral ischemia-reperfusion in rats

doi:10.3969/j.issn.1006-7795.2014.03.010

Abstract

Abstract:

Objective To observe the effect of ischemic postconditioning(IPostC) on histone deacetylase 1(HDAC1) and glial fibrillary acidic protein(GFAP) expression induced by cerebral ischemia-reperfusion injury in rats, and preliminarily explore the effect of IPostC on proliferation of astrocyte. Methods Transient middle cerebral occlusion(tMCAO) operation was performed by using suture method. A total of 21 male Sprague-Dawley(SD) rats(280-300 g) were randomly divided into 7 groups: 1 Sham group(S); 2 tMCAO 1 h group(R-1h); 3 tMCAO+IPostC 1 h group(P-1h); 4 tMCAO 4 h group(R-4h); 5 tMCAO+IPostC 4 h group(P-4h); 6 tMCAO 24 h group(R-24h); 7 tMCAO+IPostC 24 h group(P-24h). In the tMCAO+IPostC groups, IPostC was carried out by five cycles of 10 s occlusion/10 s release of the bilateral common carotid arteries using clamps immediately after reperfusion. Western blotting and immunofluorescence staining were used to observe the expression levels of HDAC1 and GFAP. Results Western blotting results showed that compared with the S group, the GFAP protein expression was increased in R groups and those in the R-1h and R-24h groups were statistically significantly increased(P<0.05). The GFAP protein expression in P groups did not change significantly. Compared with the R group, the GFAP protein expression was reduced in P groups and that in the P-4h group was statistically significantly reduced(P<0.05). Compared with the S group, the HDAC1 protein expression was increased in R groups and that in the R-1h group was statistically significantly increased(P<0.05). The HDAC1 protein expression in P groups did not change significantly. Compared with the R group, the HDAC1 protein expression in P groups was reduced clearly. The immunofluorescence staining results showed that HDAC1 was colocated with GFAP, and also were consistent with those of the Western blotting. Conclusion IPostC decreased the proliferation of astrocyte probably through decreasing HDAD1, therefore, to play a protective role in the ischemia-reperfusion injured brain.

Key words: cerebral ischemia, astrocyte, ischemic postconditioning, histone deacetylase1, rats

CLC Number:

R743.31

Gao Zhi, Zhao Haiping, Luo Yumin, Wang Rongliang, Zeng Xianwei, Ji Xunming. Ischemic postconditioning inhibited the proliferation of astrocyte following cerebral ischemia-reperfusion in rats[J]. Journal of Capital Medical University, 2014, 35(3): 310-314.

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URL: https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/10.3969/j.issn.1006-7795.2014.03.010

https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/Y2014/V35/I3/310

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