초록
본 연구는 trophic factor supplementation (TFS)이 cold ischemic storage와 rewarming 동안에 신장 세포의 생존에 미치는 효과를 알아보기 위해 실시했다. p44/42와 p38 mitogen activated protein kinases (MAPK) 활성이 TFS에 의해 영향을 받는지를 Western blot을 통해 알아보았다. Apoptotic changes를 알아보기 위해 4',6'-diamino-2-phenylindole (DAPI) 염색을 실시했다. 세포생존도를 알아보기 위해 live assay를 실시하였다. 그 결과, TFS는 cold ischemic storage와 rewarming 동안 증가된 44/42와 p38 MAPK activity를 유의성 있게 감소시켰다 (p<0.05). 또한, cold ischemic storage와 rewarming에 의한 apoptotic cell 수가 TFS에 의해 감소함을 관찰했다. 마지막으로 TFS는 유의성 있게 세포 생존도를 증가시켰다 (p<0.05). 따라서, TFS는 p44/42와 p38 MAPK 활성을 감소시키고 apoptotic change를 억제함으로써 cold ischemia와 rewarming injury로부터 신장 세포를 보호하는 것으로 생각된다.
The aim of this study was to investigate whether trophic factor supplementation (TFS) enhance the survival of kidney cell during cold ischemic storage and rewarming. The effect of TFS on the phosphorylation of p44/42 and p38 mitogen activated protein kinases (MAPK) signaling pathway was determined by Western blot. Apoptotic changes after cold ischemic storage and rewarming was determined by 4',6'-diamino-2-phenylindole (DAPI) staining. The cell viability was evaluated by live assay. TFS significantly decreased p44/42 and p38 MAPK activity induced by cold ischemic injury and rewarming (p < 0.05). The number of apoptotic cells was decreased after 5 minute rewarming in the presence of TFS. TFS significantly increased the cell viability after 5 minute rewarming (p < 0.05). Therefore, it was concluded that trophic factor supplementation protects kidney tubule cells from cold ischemic and rewarming injury via the inhibition of p44/42 and p38 MAPK activation and reducing apoptotic change.