| PrefaceSmoking is one of the most important risk factors in cerebral infarction. Still today however, we cannot explain the exact mechanism on it. Intercellular adhesion molecule - 1 ( ICAM -1) play an important role in the cerebral thrombosis. Leukocyte is adhesive to the endothelial cell (EC) conducted by ICAM - 1 ,and release some inflammatory medium, so as to cause more leukocyte adhesive to the vascular walls, becaming the basis of thrombus. We creative a model of passive smoking on Wistar rats. In situ hybridization and micrograph analyzed system were used to determin the expression of ICAM - ImRNA in rats' cerebral vascular endothelial cells, clarificating the cerebral infarction mechanism caused by smoking.Materials and methodsFifty male Wistar rats were randomly groupered into five groups: longterm - massive cigarette smoking group, longterm - morsel cigarette smoking group, shortterm - massive cigarette smoking group, anti - smoking group,normal control group. Each group has 10 Wistar rats so as to establish passive cigarette smoking models on Wistar rats. In situ hybridization and micrograph analyzed system were used to deter-min the expression of ICAM - 1mRNA in rats' cerebral vascular endo-thelial cells. Statistical analysis softwear (spss 10.0) analyzed the different expression of ICAM - ImRNA in rats'cerebral vascular endothe-lial cells among five groups.ResultsThe expression of ICAM - ImRNA was expressed in all Wistar rats'cerebral vascular endothelial cells,but seen more in those under cigarette smoking. The micrograph analyzed system shows that the expression of ICAM - 1 mRNA increased under passive smoking in rats' cerebral vascular endothelial cells. Statistical analysis (ANOVA) reports there is differential expression of ICAM - ImRNA among five groups (p < 0. 05). Couple Mean value between group comparison ( Bonferroni) shows (1) contrast to control group, except anti - smoking group, the different expression of ICAM - 1 mRNA is significant a-mong groups (p<0. 05);(2) contrast to anti - smoking groups, the different expression of ICAM - ImRNA is significant between short-term - massive cigarette smoking group and longterm - morsel cigarette smoking group(p < 0.05 ) ; (3 ) shortterm - massive cigarette smoking group contrast to longterm - morsel cigarette smoking group, the expression of ICAM - ImRNA is significant (p<0.05);(4) longterm - morsel cigarette smoking group contrast to longterm - massive cigarette smoking group, the expression of ICAM - 1 mRNA is significant (p <0.05). There are time and dose effect relationship between cigarette smoking and the expression of ICAM - ImRNA. The expression of ICAM - ImRNA was decreased in rats' cerebral vascular endothelial cells after anti - smoking and statistical analysis shows there is nosignificance versus control group( p > 0.05).ConclusionThe expression of ICAM - 1 mRNA are enhanced under cigarette smoking in rats' cerebral vascular endothelial cells. There are time and dose effect relationship between cigarette smoking and the expression of ICAM-1 mRNA.DiscussionThe structure and functions disability of endothelial cells play important rolls in the occurrence and progress during cerebral disease. Those risk factors that cause atherosclerosis, at the same time cause EC functional lesion. At present, people think that EC lesion is an early incident of atherosclerosis. EC can express much adhesive molecule , mainly including ICAM - 1, vascular cell adhesion molecule (VCAM), platelet endothelial cellular adhesion molecule ( PEC AM) , et al. Those molecules can became ligands binding leukocytes in the ischemia brain tissue .ICAM - 1 is belonged to the supper family of immune globulin, it is binded to leukocyte function - associated antigen -1 (LFA -1) mediating leukocyte adhesiving to the EC and subsequently leukocyte's transcellularing EC's roll.At normal condition, EC excretive few ICAM - 1. Although leukocyte connected to the EC, they adhesive loosely, and seperate o^iickly. Under pathologic circumstan...
|
PDF Full Text Request