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Oxidative Stress Induced PC12 Cells Damage: Roles and Mechanisms of Gap Junctional Communication
Author: WangShao
Tutor: SongZuoFeng;JingYuHong
School: Lanzhou University
Course: Human Anatomy
Keywords: Gap junctions PC12 Oxidative damage CBX Scrape-Loading AO / EB Apoptosis
CLC: R363
Type: Master's thesis
Year: 2010
Downloads: 27
Quote: 0
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Abstract
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Objective: To study shows that multiple processes involved in nerve injury gap junctions between nerve cells , but this effect is indirect or direct effect is not clear . The purpose of our research is to explore the changes of gap junctions in the process of H2O2-induced oxidative damage in PC12 cells ( rat adrenal pheochromocytoma cells) , the gap junction inhibitor CBX , whether there is a protective effect and its possible mechanism . : H2O2 for PC12 cells cultured in vitro , the successful establishment of the oxidative damage model ; Scrape-Loading Experimental evaluation of gap junctions degree of openness ; joined CBX (carbenoxolone) blocking cell gap junctions , cell viability was measured by MTT to detect the gap connection is involved in H2O2-induced oxidative damage of PC12 cells ; AO / EB staining apoptotic morphological changes and semi-quantitative apoptotic cell ratio . Results : H2O2 role in PC12 cells 4h effective lethal dose of 100 μm / L , this concentration is selected establishment of oxidative damage model , the gap between the PC12 cells concentration increased connection open ; concentration of 100μm / L and 200μm / L gap connection blocker -CBX can reduce the damage caused by H2O2 in PC12 cells ( P lt; 0.05 ) ; related to H2O2 damage effect with the start of the apoptotic signal of PC12 cells , inhibition of gap junctions open inhibit apoptosis . Conclusion : 1.H2O2 on the degree of openness of the PC12 injury and gap junction . Inhibition of gap junctions can reduce the extent of injury . 2.H2O2 cause oxidative damage of PC12 cells involves the apoptosis signal the start , to improve the role of inhibition of gap junctions open on the injury -induced apoptosis .
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