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:Ischemia microenvironment contributes mostly to the low survival rate of rat bone marrow mesenchymal stem cells after transplantation. Hydrogen sulfide (H2S) can protect various cells and tissue models against apoptosis and injury.
OBJECTIVE:To detect the cellapoptosis and viability, content of H2S in supernatant, and the expression of H2S synthetase after different time of hypoxia and serum deprivation cultivation of rat bone marrow mesenchymal stem cells.
METHODS:The passage 3 rat bone marrow mesenchymal stem cells were divided into five different cultivation time groups:0-, 3-, 6-, 12-and 24-hour groups. After enough hypoxia and serum deprivation cultivated time, the cellapoptosis was detected by SubG1, the cellviability was determined by cellcounting kit-8, the content of H 2S in supernatant was measured by N,N-dimethyl-p-phenylenediamin and the expression of H2S synthetase by RT-PCR and western blot.
RESULTS AND CONCLUSION:Compared to the normal cultivation group, after different hypoxia and serum deprivation cultivated time, the cellapoptosis increased and cellviability decreased significantly. The longer hypoxia and serum deprivation cultivated time caused the more cellapoptosis and the lower cellviability. The contents of H2S and its synthetase were also suppressed by hypoxia and serum deprivation cultivation. The difference was statistical y significant. These findings suggest that hypoxia and serum deprivation cultivation can inhibit the generation of H 2 expression of its synthetase.

BACKGROUND:Bone marrow mesenchymal stem cells (BMSCs) transplantation can promote cardiac repair after myocardial infarction, but it has been limited by the low cellsurvival rate.
OBJECTIVE:To study the effect of hydrogen sulfide (H 2 S) on the BMSCs transplantation for treatment of myocardial infarction.
METHODS:BMSCs were separated and cultivated form Sprague-Dawley rats weighing (100±20) g. The 4th generation cells were used for later experiment, and marked by DAPI at 2 hours before use. Fifty male Sprague-Dawley rats, weighing (200±20) g had been divided into five groups:Sham group (n=10) and four transplantation groups:BMSCs (n=10), H 2 S-BMSCs (n=10), H 2 S (n=10), normal saline (n=10). The myocardial infarction model of four groups was established except of sham group (only thread without ligation). The cardiac function was measured by echocardiogram at 4 weeks after celltransplantation. The col agen in the infarction area was tested by Masson staining.
RESULTS AND CONCLUSION:Severe myocardial fibrosis was found in the normal saline group, with no myocardial regeneration in the infarct area. H 2 S-BMSCs group had less col agen and more cardiac muscle tissue than BMSCs or H 2 S groups. Left ventricular ejection fraction and left ventricular fractional shortening of the H 2 S-BMSCs group were significantly higher than those of the BMSCs or H 2 S groups (P<0.05). The cells survival rate and cardiac function of myocardial infarction rats can be promoted by H 2 S-preconditioned BMSCs transplantation, which is superior to BMSCs or H 2 S alone.

Objective: To investigate the relationship between monokine induced by interferon⁃gamma (MIG) level and coronary slow flow phenomenon ( CSFP) . Methods: 80 patients diagnosed with CSFP and 54 patients with normal CAG were selected as the CSFP group and no⁃CSFP group respectively in this study. Coronary slow flow was determined quantitatively by thrombolysis in myocardial infarction (TIMI) frame count (TFC) method. The clinical characteristics and biochemical indexes , including serum CD40L and Interferon⁃γ (IFN⁃γ) , monokine induced by interferon⁃gamma (MIG) levels were measured , and the relationship between interferon⁃γ induced monocyte level and CSFP were analyzed. Results: The serum levels of CD40L , IFN⁃γand MIG in the CSFP group were higher than those in the no⁃CSFP group ( P = 0. 001) . The MIG levels were positive correlated with mean TFC ( r =0. 879 ,P = 0. 009) . Multivariate logistic regression analysis showed that MIG was an important risk factor for CSFP (β = 0. 874 ,P = 0. 011) . The ROC curve analyses indicated that the MIG levels had diagnostic value in patients with CSFP , the area under the curve ( AUC) was 0. 793 , the sensitivity was 0. 79% and the specificity was 76. 0% , and 95% CI 0. 714 - 0. 872. Conclusion Chemokine CD40L , IFN⁃ γ and MIG may be involved in the process of vascular inflammation and arteriosclerosis. MIG is an important influencing factor of CSFP and participated in the occurrence and development of CSFP.