Smoking Treatment Increase Serum AGEs Level And Have Effects On Expression Of Icam-1 In Vascular Endothelial Cells Of Rat

Objective:To investigate whether smoking can increase serum advanced glycosylation end products (AGEs) level and have the effects of on expression of intercellular cell adhesion molecule-1 (ICAM-1) in vascular endothelial cells of rat; to evaluate the role of aminoguanidine and puerarin in this process; to explore probably mechanism which smoking affect expression of ICAM-1 in vascular endothelial cells and to provide experimental evidence for clinic to seek available management.Methods:Male SD rats (n=138) were randomly assigned to five groups according to duration of smoking treatment: two-week group (2w group, n=30), four-week group (4w group, n=30), six-week group (6w group, n=30), eight-week group (8w group, n=30), smoking cessation group (sc group, n=18). The rats of following groups, i.e. 2w, 4w, 6w and 8w groups were further randomly divided into five subgroups according to intervening condition: control subgroup(CON subgroup, n=6), smoking treatment for 1h/per day subgroup(SM1 subgroup, n=6), smoking treatment for 0.5h/per day subgroup (SM2 subgroup, n=6), aminoguanidine hydrochloride subgroup (AG subgroup, n=6), puerarin subgroup (PU subgroup, n=6); the rats of smoking cessation group were further randomly divided into three subgroups according to duration of smoking cessation: smoking cessation two weeks subgroup(n=6), smoking cessation four weeks subgroup (n=6) and smoking cessation six weeks subgroup (n=6). Except for the rats of control subgroups, all rats were given smoking treatment in an airproof box of 72L size. "Fei-ma" cigarette was utilized, and the density of smoke in the box was 5%. The rats of SM2 subgroup were given smoking treatment for 0.5 h/per day, others for 1h/per day, rats of AG subgroup and PU subgroup were synchronously given aminoguanidine hydrochloride and puerarin respectively. The rats of 2w, 4w, 6w and 8w groups were sacrificed after smoking treatment for two, four, six and eight weeks respectively; the rats of smoking cessation group were sacrificed after smoking treatment for eight weeks and then cease-smoking for two, four, and six weeks respectively. Serum AGEs levels of each rat were assayed by fluorescent method. ICAM-1 mRNA and protein of vascular endothelial cells were determined by semiquantitative RT-PCR (Reverse transcription polymerase chain reaction) and immunohistochemistry. Results:Serum AGEs levels of all SM1 subgroups rats were increased after smoking treatment for two weeks (p<0.01), and reached peak at four weeks (p<0.001), then declined at six weeks and eight weeks, but did not recovere back to normal level; the increasing trend was depressed by aminoguanidine hydrochloride and puerarin. Levels of serum AGEs declined in smoking cessation rats, and were significantly lower at four weeks than those before smoking cessation (p<0.001). With the increased duration of smoking, ICAM-1 mRNA and protein of vascular endothelial cells were up-regulated, both aminoguanidine hydrochloride and puerarin depress the up-regulation. The expression of ICAM-1 mRNA and protein of vascular endothelial cells also declined after smoking cessation, and they were significantly lower in rats of smoking cessation of four weeks subgroup than those before smoking cessation (p<0.05).Conclusions:Smoking treatment increase serum AGEs level in rat. Cigarette-induced AGEs play roles in the augmented expression of ICAM-1 in vascular endothelial cells of rat with smoking treatment. Aminoguanidine hydrochloride, puerarin and smoking cessation contribute to the decrease of serum AGEs level and the expression of ICAM-1 in vascular endothelial cells of rat.