| BACKGROUD and AIM: Cardiovascular disease is the leading cause of mortality worldwide. Atherosclerosis constitutes the main pattern of cardiovascular disease and leads to thickening of the intima with plaque formation and eventual occlusion of the arterial lumen. A large amount of evidence links advanced glycation end products (AGEs) with the development or progression of atherosclerosis, regardless of the diabetic status. AGEs are a heterogenous group of compounds formed by the nonenzymatic reaction of reducing sugars with proteins, lipids, and nucleic acids. Although AGEs are formed endogenously in the body, smoking has recently been recognized as an important exogenous source.Peroxisome proliferator activated receptor γ(PPARγ) is a ligand-inducible transcription factor that belongs to the nuclear hormone receptor superfamily. PPARγ is expressed in atherosclerotic lesions and has been shown to affect transcription of genes in vascular endothelial cells, smooth muscle cells, monocytes, and monocyte-derived macrophages. The down-regulation of several atherogenic genes by PPARγactivation suggests that stimulation of PPARγ expression and/or activation may have beneficial effects on the progress of atherosclerotic disease.Aminoguanidine, a nucleophilic hydrazine compound, prevents AGEs formation by mechanisms that involve trapping of reactive dicarbonyl intermediates in the Maillard reaction. Puerarin has been shown to inhibit aldose reductase, non-enzymatic glycation, to clear away AGEs and reactive oxygen species.The aim of this study is to observe the effects of smoking on rat serum AGEs and expression of PPARγ in rat aorta, and to assess the effects of aminoguanidine and puerarin.METHODS: Male SD rats (n = 120) were randomly assigned to four groups by the duration of smoking : 2 weeks group (n=30), 4 weeks group (n=30), 6 weeks group (n=30), 8 weeks group (n=30). The rats of each group again were randomly assigned to five subgroups by intervene condition: control subgroup (CON, n=6), smoking 1 h/d subgroup (SM1, n=6), smoking 0.5 h/d subgroup (SM2, n=6), smoking and aminoguanidine subgroup (AG, n=6), smoking and puerarin subgroup (PU, n=6). Except for the rats of CON subgroup, all rats passively smoke in a airproof box whose cubage is 72 L. Fei-ma cigarette was utilized, and the density of smoke in the box was 5%. The rats of SM2 subgroup smoke 0.5 h/d, others smoke 1 h/d, rats of AG subgroup and PU subgroup were given aminoguanidine and puerarin respectively. The rats were killed after two weeks, four weeks, six weeks and eight weeks of smoking respectively. The serum AGEs level of each rat was assayed by fluorescent method. PPARγmRNA and protein were determined by semi-quantitative RT-PCR and immunohistochemistry.RESULES:1.No changes of serum levels of glucose and lipid were observed in SD rats after smoking.2.It was found that serum AGEs level increased in SD rats after two weeks of smoking, and it reached the peak at fourth week, then it decreased slightly at sixth and eighth week. The serum AGEs level of SD rats of SM2, AG and PU subgroups was lower than that of SD rats of SM1 subgroup.3.For light microscopy, no difference was observed in aorta slices stained with HE reagent in SD rats of 8 weeks group. But they appeared expression of early atherosclerosis for electron microscopy.4.The PPARγ mRNA and protein levels decreased in SD rats after smoking, in a time-related manner. The PPARγ mRNA and protein levels of SD rats of SM2, AG and PU subgroups were higher than that of SD rats of SM1 subgroup.CONCLUTIONS:1.Serum AGEs level of SD rats increased after smoking, and no changes of the serum levels of glucose and lipid were found.2.Expression of PPARγ in rats aorta decreased after smoking, in a time-related manner.3.Both aminoguanidine and puerarin deceased serum AGEs level, and enhanced expression of PPARγ.
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