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Basic science: Cardiovascular disease basic research
e0155 Smoking treatment increase serum AGEs Level and have effects on expression of ICAM-1 in vascular endothelial cells of rat
  1. Yungen Jiao,
  2. Naifen Liu
  1. Cardiovascular Institute of Southeast University, Nanjing, China

Abstract

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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