Changes of neuronic apoptosis, Rho GDP dissociation inhibitor 2 and Bcl-2 in brain tissue of neonatal rats with hypoxic-ischemic brain damage

Abstract

Objective To investigate the effect of Rho GDP dissociation inhibitor 2 （RhoGDI2） and Bcl-2 in pathogenesis of hypoxic-ischemic brain damage （HIBD）. Methods Neonatal 7-day-old Sprague Dawley rats were randomly divided into sham-operation control group, HIBD 6 h group and HIBD 48 h group （ n = 10 per group）. The apoptosis rate of brain cell was measured by flow cytometer and the expression of RhoGDI2 mRNA and Bcl-2 mRNA were detected by Real-time RT-PCR. Results （ 1 ） The ligated cerebral hemisphere of neonatal rats showed obvious edema at 48 h after hypoxia-ischemia. （ 2 ） Apoptotic cell appeared at 6 h in HIBD group,the apoptosis rate was （ 1.40 ±0. 12） %. The apoptosis rate obviously increased to （ 15.86 ±0.98 ） % at 48 h after HIBD, which showed a significant increase compared to sham-operation control group （ P 〈 0.01 ）. （ 3 ） The expressions of both RhoGDI2 mRNA and Bcl-2 mRNA were 4. 12 ±0. 74 and 2. 55±0. 65 respectively in sham-operation control group. In HIBD group, the expressions of both RhoGDI2 mRNA and Bcl-2 mRNA began to decrease at 6 h after HIBD （3. 19±0. 77,1.96±0. 36） and decreased furthermore at 48 h after HIBD （ 1.04±0. 18,1.06 ±0. 17 ）. The differences of expression levels among three groups were statistically significant （P 〈 0. 01 ）. （4） The expression of RhoGDI2 mRNA positively correlated with the expression of Bcl-2 mRNA （ r = 0. 831, P 〈 0. 05 ）. Conclusion With the emerging of apoptosis after HIBD, the expressions of both RhoGDI2 mRNA and Bcl-2 mRNA are decreased. The imbalance of expression of RhoGDI2 is involved in pathogenesis of HIBD by regulating Bcl-2 expression. Key words: Hypoxic-ischemic brain damage; Rho GDP dissociation inhibitor 2 ; Bcl-2 ; Apoptosis ; Rat, newborn