CONTEXT: Atorvastatin is a member of the drug class known as statins, which is used for lowering blood cholesterol. OBJECTIVE: The present study investigates the effect and mechanism of atorvastatin on neointimal hyperplasia after carotid artery injury (CAI) of rat. MATERIALS AND METHODS: Fifty male rats were randomly divided into four groups: control group, sham-operated group, model group, and atorvastatin treatment group. The treatment group was fed with atorvastatin (10 mg/kg) with gastro-gavage at 5 p.m. every day for 28 d after surgery. The control group, model group, and sham-operated group were fed with the same volume of distilled water instead. The proliferations of intimal and medial layers were evaluated by hematoxylin & eosin (H&E) staining. The apoptosis of vascular smooth muscle cells (VSMCs) was determined by terminal deoxynucleotidyl transferased UTP nick end labeling (TUNEL) staining. Plasma concentrations of survivin and sFas were detected by enzyme-linked immunosorbent assay (ELISA). RESULTS: Atorvastatin reduced neointimal formation and increased apoptosis of VSMCs in neointima. VSMCs apoptosis emerged at 3 d (8.42 ± 0.449 μm) and the intimal proliferation peaked by the end of 14 d (41.58 ± 1.64 μm). The plasma levels of survivin and sFas were gradually increased with the neointimal hyperplasia and increasingly decreased after atorvastatin treatment. The plasma levels of survivin and sFas in rats were elevated at 3 d (464.80 ± 105.27 pg/ml and 3256.00 ± 478.20 pg/ml, respectively), reached the peak of survivin at 14 d (1089.20 ± 232.32 pg/ml) and sFas at 7 d (4362.00 ± 639.92 pg/ml) and decreased at 28 d (562.00 ± 90.11 pg/ml and 2148.00 ± 257.14 pg/ml, respectively) in the model group. Compared with the model group, the atorvastatin treatment group has significantly less neointimal hyperplasia and more apoptosis of VSMCs. CONCLUSIONS: Atorvastatin can inhibit neointimal hyperplasia and promote SMCs apoptosis in neointimal layers, which may be mainly associated with down-regulation of survivin and Fas expression after CAI of rat.
CONTEXT: Atorvastatin is a member of the drug class known as statins, which is used for lowering blood cholesterol. OBJECTIVE: The present study investigates the effect and mechanism of atorvastatin on neointimal hyperplasia after carotid artery injury (CAI) of rat. MATERIALS AND METHODS: Fifty male rats were randomly divided into four groups: control group, sham-operated group, model group, and atorvastatin treatment group. The treatment group was fed with atorvastatin (10 mg/kg) with gastro-gavage at 5 p.m. every day for 28 d after surgery. The control group, model group, and sham-operated group were fed with the same volume of distilled water instead. The proliferations of intimal and medial layers were evaluated by hematoxylin & eosin (H&E) staining. The apoptosis of vascular smooth muscle cells (VSMCs) was determined by terminal deoxynucleotidyl transferased UTP nick end labeling (TUNEL) staining. Plasma concentrations of survivin and sFas were detected by enzyme-linked immunosorbent assay (ELISA). RESULTS:Atorvastatin reduced neointimal formation and increased apoptosis of VSMCs in neointima. VSMCs apoptosis emerged at 3 d (8.42 ± 0.449 μm) and the intimal proliferation peaked by the end of 14 d (41.58 ± 1.64 μm). The plasma levels of survivin and sFas were gradually increased with the neointimal hyperplasia and increasingly decreased after atorvastatin treatment. The plasma levels of survivin and sFas in rats were elevated at 3 d (464.80 ± 105.27 pg/ml and 3256.00 ± 478.20 pg/ml, respectively), reached the peak of survivin at 14 d (1089.20 ± 232.32 pg/ml) and sFas at 7 d (4362.00 ± 639.92 pg/ml) and decreased at 28 d (562.00 ± 90.11 pg/ml and 2148.00 ± 257.14 pg/ml, respectively) in the model group. Compared with the model group, the atorvastatin treatment group has significantly less neointimal hyperplasia and more apoptosis of VSMCs. CONCLUSIONS:Atorvastatin can inhibit neointimal hyperplasia and promote SMCs apoptosis in neointimal layers, which may be mainly associated with down-regulation of survivin and Fas expression after CAI of rat.
Authors: Ali F AbuRahma; Mohit Srivastava; Patrick A Stone; Bryan K Richmond; Zachary AbuRahma; Will Jackson; L Scott Dean; Albeir Y Mousa Journal: J Am Coll Surg Date: 2014-12-15 Impact factor: 6.113