不同潜伏期致痫大鼠海马神经元线粒体损伤及Fas和Bax表达

Mitochondrial damage and expressions of Fas and Bax in the hippocampal neurons after status epilepticus of different latencies in rats

目的观察不同潜伏期致癫痫持续状态(SE)大鼠海马区神经元线粒体超微结构损伤及Fas和Bax的表达。方法分别采用海人酸腹腔注射(A组)和尾静脉注射(B组)诱发不同潜伏期的大鼠SE。于SE终止后3、6、24、48、72点取海马,电镜观察线粒体的超微结构,半定量RTPCR检测Fas、Bax的mRNA表达。另取10只不作任何处理的大鼠作为正常对照组。结果A组潜伏期为97±11min,线粒体肿胀,神经元呈凋亡征;B组潜伏期为48±13min,线粒体肿胀且伴膜的崩解,神经元呈坏死表现。B组Fas及BaxmRNA的表达与对照组相比无明显差异(P>0.05);与对照组相比A组Fas及BaxmRNA表达均于SE后6h增加(P<0.05),48h达高峰(P<0.001),并持续至72h(P<0.001)。结论不同潜伏期的SE导致了不同程度的线粒体损伤,进而决定了神经元死亡的分子机制。

Objective To observe the mitochondrial ultrastructure damage and mRNA expressions of Fas and Bax in the hippocampal neurons after status epileptieus （SE） of different latencies in rats. Methods SE was induced by intraperitoneal injection of 12 mg/kg kanic acid （Group A） or tail vein injection of 10 mg/kg kanic acid （Group B） in rats. The rats were killed 3, 6, 24, 48 and 72 hrs after SE and the hippocampus were taken out. The mitochondrial ultrastructures were observed under an electron microscope. Fas and Bax mRNA were determined by semiquantitative RT-PCR. Ten rats without any treatment were used as the control group. Results The latency was 97 ± 11 min, and the swelling mitochondrion and apoptotic neurons were observed in Group A. The latency was 48 ± 13 min, the mitoehondrion were swelling with ruptured membrane, and the neurons were necrotic in Group B. Fas and Bax mRNA began to increase at 6 hrs after SE, reached a peak at 48 hrs and remained higher at 72 hrs in Group A compared with the control group. There were no differences in Fas and Bax expressions between Group B and the control group. Conclusions SE of different latenciees resulted in different degrees of mitochondrial damages, which determined the molecular mechanisms of neuronal death.