肾上腺功能水平对脑缺血再灌注大鼠海马bax和bcl-2基因表达的影响

Effects of adrenal gland on the expression of bax and bcl-2 in hippocampus after cerebral ischemia

目的:观察肾上腺功能水平对大鼠脑缺血再灌注后海马bax和bcl-2基因表达的影响。方法:成年雄性Wistar大鼠36只随机分为单侧肾上腺切除组(ADX)、单侧肾上腺切除+注射糖皮质激素组(GC)和假手术对照组(sham)。所有大鼠在单侧肾上腺切除或假手术14d后行全脑再灌注手术。每组大鼠分别于再灌注后1h、4h、8h、24h随机取3只断颈处死,取海马组织提取总RNA,RT-PCR半定量检测c-fos、bax和bcl-2的表达情况。另设3只大鼠为正常组(normal)。结果:c-fos、bax表达水平在ADX、GC、sham3组之间无统计学差异(P>0.05)。Sham组bcl-2表达水平明显高于ADX组和GC组(P<0.05),而ADX组与GC组bcl-2表达无统计学差异(P>0.05)。Sham组bax/bcl-2明显低于ADX组和GC组(P<0.05),而ADX组与GC组间bax/bcl-2无统计学差异(P>0.05)。结论:肾上腺功能水平对脑缺血再灌注后大鼠海马组织c-fos和bax基因表达无影响,但肾上腺功能低下会导致脑缺血再灌注后大鼠海马组织bcl-2基因表达下调,bax/bcl-2比值升高,可能促进海马组织细胞发生凋亡,补充糖皮质激素对此bcl-2基因表达下调无纠正作用,表明还有其它机制存在。

AIM： To observe the effects of adrenal gland on the hippocampus responses to cerebral ischemia. METHODS ： 36 Wistar rats were randomly divided into three groups ： sham - operated control group （ sham ）, unilateral adrenalectomy were performed in ADX and GC group, and GC group were injected with 5 mg/per rat of dexamethasone before cerebral ischemia. Fourteen days after the first operation, all animals were performed occlusion of bilateral carotid artery for 15 min, and then reperfusion. 3 rats of each group were sacrificed at 1 h, 4 h, 8 h and 24 h after reperfusion and hippocampus were dissected. The total RNA was rapidly extracted from hippocampus tissue. The expressions of c -fos, bcl - 2 and bax gene were quantified with the method of semiquantitive RT - PCR. RESULTS ： The expressions of c -fos and bax in three groups showed no statistical differences （ P 〉 0. 05 ）. The expression of bcl - 2 in sham group was significantly higher than that in GC and ADX groups （ P 〈 0.05）. However, no differences of bcl - 2 expression between GC and ADX group （ P 〉 0. 05 ） was observed. The ratio of bax to bcl - 2 in sham group was significantly lower than that in GC and ADX groups （ P 〈 0. 05）, no significant differences of the ratio displayed between ADX and GC group. CONCLUSION： The expression of c -fos and bax in hippocampus after cerebral ischemia is not affected by adrenal gland. The excision of unilateral adrenal gland downregnlates bcl - 2 expression and raises the ratio of bax to bcl - 2 in rat hippocampus after cerebral ischemia. Dexamethasone treatment does not alter the expression of bcl - 2 in ADX and GC groups. The results indicate that the adrenal gland can counteract cell apoptosis in hippocampus tissue induced by cerebral ischemia. Adrenal steroids are not sufficient to enable the compensatory increase in bcl - 2 expression in steroid - deficient animal, some other mechanism may exist.