广东医学2012，Vol.33Issue(8)：1046-1049,4.
右美托咪定对抗化学性低氧引起神经细胞的损伤及其机制
The protection of dexmedetomidine against chemical hypoxia-induced neurons injury and its mechanism
林琳 1兰爱平 2张莉莉 1周舸 1华潇潇 1刘明姬 1冯鉴强 2莫利求1
作者信息
- 1. 中山大学附属第一医院黄埔院区麻醉科,广州,510700
- 2. 中山大学中山医学院生理学教研室,广州,510080
- 折叠
摘要
Abstract
Objective To investigate whether α2 - adrenoreceptor agonist dexmedetomidine ( Dex) protects PC12 cells against chemical hypoxia - induced injury by inhibiting p38MAPK pathway. Methods PC12 cells were treated with cobalt chloride ( CoCl2) to establish a model of chemical hypoxia - induced neuronal injury. Expression of p38 mitogen -activated protein kinase ( MAPK) protein was measured by Western blot assay. Cell viability was assessed by cell counter kit (CCK -8). The changes in morphology and the apoptotic cell count were observed by Hoechst 33258 staining. Mito-chondrial membrane potential ( MMP) was measured by rhodaminel23 staining and photofluorography. Results Exposure of PC12 cells to 600 μmol/L CoCl2 significantly enhanced the expression of phosphorylated(p) p38MAPK at the duration between 60 and 180 min, peaking at 120 min. Dex at 400 μmol/L not only protected PC12 cells against CoCl2 - induced cytotoxicity, apoptotic effect and MMP damage, but also inhibited up - regulation of p - p38MAPK induced by CoCl2. SB203580, an inhibitor of p38MAPK, mimicked the neuroprotective effect of Dex against chemical hypoxia - induced injury, evidenced by increases in both cell viability and MMP, as well as decrease in apoptotic cells. Conclusion Dex can protect neuronal cells against chemical hypoxia - induced injury, inhibition of p38MAPK pathway may be one of the mechanisms responsible for this effect.关键词
右美托咪定/p38MAPK通路/PC12细胞/氯化钴/凋亡Key words
dexmedetomidine/p38 mitogen -activated protein kinase pathway/PC12 cells/cobalt chloride/ap-optosis引用本文复制引用
林琳,兰爱平,张莉莉,周舸,华潇潇,刘明姬,冯鉴强,莫利求..右美托咪定对抗化学性低氧引起神经细胞的损伤及其机制[J].广东医学,2012,33(8):1046-1049,4.
