Activation of NF-kappaB and apoptosis of intestinal epithelial cells induced by hydrogen peroxide.
- Author:
	        		
		        		
		        		
			        		Jianming LI
			        		
			        		
			        		
			        			1
			        			
			        		
			        		
			        		
			        		
			        		;
		        		
		        		
		        		
			        		Hong ZHOU
			        		
			        		;
		        		
		        		
		        		
			        		Qian CAI
			        		
			        		;
		        		
		        		
		        		
			        		Guangxia XIAO
			        		
			        		
		        		
		        		
		        		
			        		
			        		Author Information
			        		
 - Publication Type:Journal Article
 - MeSH: Apoptosis; Humans; Hydrogen Peroxide; toxicity; Intestinal Mucosa; metabolism; Microscopy, Confocal; NF-kappa B; metabolism; Reactive Oxygen Species; toxicity; Tumor Cells, Cultured
 - From: Chinese Journal of Traumatology 2002;5(4):209-213
 - CountryChina
 - Language:English
 - 
		        	Abstract:
			       	
			       		
				        
				        	
OBJECTIVEIn vitro model of hydrogen peroxide induced apoptosis of SW-480 cells was used to investigate the role of NF-kappaB in the pathogenesis of reactive oxygen species induced apoptosis of intestinal epithelial cells.
METHODSUltra-structural changes were observed. Apoptosis of SW-480 cell line was determined by Annexin-V and PI double-stained flow cytometry. Nuclear translocation of NF-kappaB was determined by anti-NF-kappaB polyclonal antibody and EB double-staining. NF-kappaB activity was studied by electrophoretic mobility shift assays. RT-PCR was performed to study expression of NF-kappaB mRNA.
RESULTSHydrogen peroxide led to apoptosis of SW-480 cells, condensed or semilunar chromatin even apoptotic bodies could be observed. Nuclear translocation of NF-kappaB, increase of NF-kappaB activity and expression of NF-kappaB mRNA were found simultaneously.
CONCLUSIONSEarly activation of NF-kappaB may be one of the mechanisms of apoptosis in intestinal epithelial cells by reactive oxygen species.
 
            