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| 在不同发育阶段亲环素D在缺血缺氧性脑损伤中的作用 |
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| Developmental shift of cyclophilin D contribution to hypoxic-ischemic brain injury |
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| Wang X., Carlsson Y., Basso E., Zhu C., Rousset C.I., Rasola A., Johansson B.R., Blomgren K., Mallard C., Bernardi P., Forte M.A., Hagberg H. 2009/5/29 18:40:20 |
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Journal of Neuroscience, 2009, Volume 29, Issue 8
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| Cyclophilin D (CypD), a regulator of the mitochondrial membrane permeability transition pore (PTP), enhances Ca2+-induced mitochondrial permeabilization and cell death in the brain. However, the role of CypD in hypoxic-ischemic (HI) brain injury at different developmental ages is unknown. At postnatal day (P) 9 or P60, littermates of CypD-deficient [knock-out (KO)], wild-type (WT), and heterozygous mice were subjected to HI, and brain injury was evaluated 7 d after HI. CypD deficiency resulted in a significant reduction of HI brain injury at P60 but worsened injury at P9. After HI, caspase-dependent and-independent cell death pathways were more induced in P9 CypD KO mice than in WT controls, and apoptotic activation was minimal at P60. The PTP had a considerably higher induction threshold and lower sensitivity to cyclosporin A in neonatal versus adult mice. On the contrary, Bax inhibition markedly reduced caspase activation and brain injury in immature mice but was ineffective in the adult brain. Our findings suggest that CypD/PTP is critical for the development of brain injury in the adult, whereas Bax-dependent mechanisms prevail in the immature brain. The role of CypD in HI shifts from a predominantly prosurvival protein in the immature to a cell death mediator in the adult brain. Copyright © 2009 Society for Neuroscience. |
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| Correspondence Address: Wang, X.; Perinatal Center, Department of Physiology, University of Gothenburg, 30 Gothenburg, SE-405, Sweden; email: xiaoyang.wang@fysiologi.gu.se |
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 疾病资源中心
摘自：《西氏内科学》，第23版
患者女性，21岁，因干咳、间歇性气促2个月到急诊科就诊。开始症状为上呼吸道感染引起的鼻塞、流涕和咳嗽。医生检查后开了抗生素。服药后鼻部症状缓解，但仍有轻微干咳和呼吸困难。其他症状包括疲劳和焦虑。否认发热、体重减轻、胸痛、端坐呼吸、气喘、鼻后滴漏、胃灼热以及神经系统症状。
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