Objective To investigate whether smoking can increase serum advanced glycosylation end products (AGEs) level and have effects on expression of intercellular cell adhesion molecule-1 (ICAM-1) in vascular endothelial cells of rat.
Methods Male SD rats (n=138) were randomly assigned to five groups according to duration of smoking treatment: 2-week group, 4-week group, 6-week group, 8-week group, smoking cessation group. The rats of following groups, that is 2w, 4w, 6w and 8w groups were further randomly divided into five subgroups according to intervening condition: control subgroup, smoking treatment for 1 h/per day subgroup, smoking treatment for 0.5 h/per day subgroup, aminoguanidine hydrochloride subgroup, puerarin subgroup; the rats of smoking cessation group were further randomly divided into three subgroups according to duration of smoking cessation: smoking cessation 2 weeks subgroup, smoking cessation 4 weeks subgroup and smoking cessation 6 weeks subgroup. The rats of 2w, 4w, 6w and 8w groups were sacrificed after smoking treatment for 2, 4, 6 and 8 weeks respectively; the rats of smoking cessation group were sacrificed after smoking treatment for 8 weeks and then cease-smoking for 2, 4, and 6 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 PCR) and immunohistochemistry.
Results Serum AGEs levels of all SM1 subgroups rats were increased after smoking treatment for 2 weeks (p<0.01), and reached peak at 4 weeks (p<0.001), then declined at 6 weeks and 8 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 4 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 4 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.
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