Abstract:

Objective To study the effects of artemisinin on intimal hyperplasia in autogenous vein grafts in rats. Methods Jugular vein⁃to⁃artery bypass grafting was performed on 32 male Sprague⁃Dawley rats.The rats were randomly divided into two groups：the treatment group（n = 16）and the control group（n = 16）. The treatment group was given gastric perfusion artemisinin 100 mg/（kg · d）which began 1 day before operation and continued until harvesting，and the control group was given to the same volume with normal saline by the same way. At 2 or 4 weeks after surgery，vein grafts were harvested，with 8 rats for each time point. Computer image analysis system was applied tocalculate the thickness of neointima in the vein grafts，expression area of smooth muscle 22α（SM22α）was identi⁃ fied by immunohistochemical observationand the protein level of SM22α was detected by Western bolt. Results After 2 or 4 weeks，neointima thickness of the vein graft in the treatment group was significantly reduced compared with that of the control group［（20.79 ± 1.88）μm vs.（35.23 ± 2.66）μm，P＜0.01；（37.06 ± 2.22）μm vs.（46.23 ± 2.54）μm，P＜0.01］. The expression of SM22α protein was detected in smooth muscle cells of vein graft after surgery. The positive rate of SM22α protein expression were significantly inhibited in the treatment group than that of the control group［（59.20 ± 5.76）vs.（26.12 ± 3.72），P＜0.01；（35.63 ± 4.36）vs.（10.38 ± 2.98），P＜0.01］. The protein expression levels of SM22α（SM22α/β ⁃Actin）were significantly inhibitedin the treatment group than that of the control group［（0.58 ± 0.1）vs.（0.39 ± 0.06），P＜0.01；（0.42 ± 0.06）vs.（0.21 ±0.05），P＜0.01］. Conclusion Artemisinin could obviously inhibit hyperplasia of intimal thickness after venous transplantation，which may be relat⁃ ed to inhibit the lower the expression of SM22α and inhibition of smooth muscle cell proliferation.

Key words: artemisininsmooth,  , muscle 22α,  , intimal hyperplasia,  , restenosis