Relationship between nicotine stimulation and transforming growth factor-beta 1 expression in apolipoprotein E gene knockout mice

Background: Studies have shown that nicotine can induce atherosclerosis. But its specific mechanisms remain unclear. Objective: To explore the relationships between the formation of atherosclerotic plaque and the level of peripheral blood transforming growth factor-beta 1 in apolipoprotein E gene knockout mice following the stimulation of different doses of nicotine Methods: ApoE gene knockout mice were peritoneally injected with two different doses of nicotine (2 and 0.5 mg/kg/d) for 12 weeks as high-dose nicotine group and low-dose nicotine group, respectively. The mice of the control group were injected with an equal volume of normal saline. The level of peripheral blood transforming growth factor-beta 1 was detected by enzyme-linked immunosorbent assay, and pathological changes of atherosclerotic plaque were observed by hematoxylin-eosin staining. Results and Conclusion: After 12 weeks of nicotine treatment, the level of peripheral blood transforming growth factor-beta 1 in the low-dose nicotine group was lower than that in the control group (P < 0.05). The level of peripheral blood transforming growth factor-beta 1 in the high-dose nicotine group was lower than that in the control group and low-dose nicotine group (P < 0.05). In addition, the degree of vascular stenosis in the high-dose nicotine group was the most serious followed by the low-dose nicotine group and the control group. There was significant difference among the three groups (P < 0.05). Besides, the number of plaques in the low-dose and high-dose nicotine groups was more than that in the control group (P < 0.05). There was no significant difference in the number of plaques between the low-dose nicotine group and high-dose nicotine group (P > 0.05). Moreover, there was a negative correlation between vascular stenosis rate and transforming growth factor-beta1 level (r=-0.920, P=0.000). There results suggest that nicotine stimulation can increase the number of atherosclerotic plaques in ApoE gene knockout mice, which may be related to the inhibitory effect of nicotine on transforming growth factor-beta1 level.