BACKGROUND:Inflammation plays an important role in vessel proliferation after balloon injury.Reducing inflammatory reaction may lighten the ocurrence and development of the restenosis after angioplasty.Studies have demonstrated that PPAR? excitomotor has inhibitory effects on inflammation development.OBJECTIVE:To observe the changes in inflammatory factors after carotid artery balloon injury in rats and the intervention of PPAR? excitomotor rosiglitazone.DESIGN,TIME AND SETTING:The randomized,controlled animal experiment was performed at the Central Laboratory of Shenzhen People's Hospital from January to June 2009.MATERIALS:Male SPF SD rats weighing about 350 g were selected to generate models of carotid balloon injury.METHODS:SD rats were equally and randomly divided into 3 groups:the control group,the balloon injury group and the rosiglitazone group.The left common carotid arteries were injured by balloon in the balloon injury group and the rosiglitazone group.The control group received sham operation.The rosiglitazone group was administered rosiglitazone daily by gavage,which began 4 days before operation and continued until harvesting.Accordingly,the control group and the balloon injury group were administered normal saline daily by gavage.MAIN OUTCOME MEASURES:All rats were executed under anesthesia at 14 days after operation,respectively to harvest left common carotid artery samples.The vessels were stained by hematoxylin-eosin,and Neointimal area(NIA) and media area(MA) as well as NIA/MA were calculated.Real time RT-PCR and Western Blot method were used to assay the expression of interleukin(IL)-6,IL-10,IL-17A mRNA and the distribution of nuclear factor(NF)-?B protein.RESULTS:Of the 36 rats,5 were excluded due to failed modeling or death,and 31 rats were included in final analysis.①The expression levels of IL-6 and IL-17A mRNA in the rosiglitazone group were significantly lower than the balloon injury group,but higher than the control group(P

BACKGROUND:Restenosis and lumina loss limit further application of balloon extension and stent implantation.Effect of tunica intima proliferation and apoptosis in restenosis and the intervention method are exploring.OBJECTIVE:To investigate the influence of Rosuvastatin on the vascular smooth muscle cells proliferation and apoptosis in rats with carotid artery injury established by Medtronic balloon.METHODS:The male SD rats were randomly and equally divided into injury group and treatment group.Each rat was subjected to balloon injury on the lift common carotid artery,and control artery without balloon injury on the right artery served as control group.Treatment group rats were given Rosuvastatin(dissolved in Nacl)5 mg/kg per day 3 days before injury,while the injury group rats were given 9 g/L NaCl.At 7 and 14 days after injury,the common carotid arteries were harvested for HE staining.SM α-actin and proliferating celI nuclear antigen were detected by immunohistochemistry.In addition,smooth muscle cells apoptosis was detected by TUNEL.RESULTS AND CONCLUSION:The neointimal area and the area ratio of neointimal/media were decreased in treatment grouP significantly at 14 days compared with injury group(P<0.05),and neointimal area increased by 26%:positive cell rate of proliferating cell nuclear antigen was decreased,but apoptosis cells were increased cornpared with the injury group(P<0.05).Results showed that Rosuvastatin prior to balloon injury inhibited neointimal proliferation and neointimal celI proliferation following balloon Injury,promoted smooth muscle cells apoptosis,ultimately reducing neointimaI formation and inhibiting restenosis.

BACKGROUND: Inflammation plays an important role in vessel proliferation after balloon injury. Reducing inflammatory reaction may lighten the ocurrence and development of the restenosis after angioplasty. Studies have demonstrated that PPAR_Y excitomotor has inhibitory effects on inflammation development. OBJECTIVE: To observe the changes in inflammatory factors after carotid artery balloon injury in rats and the intervention of PPARy excitomotor rosiglitazone. DESIGN, TIME AND SETTING: The randomized, controlled animal experiment was performed at the Central Laboratory of Shenzhen People's Hospital from January to June 2009. MATERIALS: Male SPF SD rats weighing about 350 g were selected to generate models of carotid balloon injury. METHODS: SD rats were equally and randomly divided into 3 groups: the control group, the balloon injury group and the rosiglitazone group. The left common carotid arteries were injured by balloon in the balloon injury group and the rosiglitazone group. The control group received sham operation. The rosiglitazone group was administered rosiglitazone daily by gavage,which began 4 days before operation and continued until harvesting.Accordingly,the control group and the balloon injury group were administered normal saline daily by gavage. MAIN OUTCOME MEASURES: All rats were executed under anesthesia at 14 days after operation, respectively to harvest left common carotid artery samples. The vessels were stained by hematoxylin-eosin, and Neointimal area (NIA) and media area (MA) as well as NIA/MA were calculated. Real time RT-PCR and Western Blot method were used to assay the expression of interleukin (IL)-6, IL-10, IL-17A mRNA and the distribution of nuclear factor (NF)-kB protein. expression levels of IL-6 and IL-17A mRNA in the rosiglitazone group were significantly lower than the balloon injury group, but higher than the Control group( P < 0.05), The expression levels of IL-10 mRNA in the rosiglitazone group were higher than the the rosiglitazone group was down-regulated, and lower than the balloon injury group, but higher than control group (P < 0.05). CONCLUSION: Rosiglitazone can regulate the expression of II-6 IL-10 IL-17A mRNA and the balance of inflammatory factors via NF-kB,inhibit the inflammatory reaction of injured vessels and may contribute to lighten the restenosis of injured vessels.