The relation between the expression and activity of MMP-9 in C-reactive protein (CRP)-induced human THP-1 mononuclear cells and the activation of nuclear factor kappa-B (NF-kappaB) was studied to investigate the possible role of CRP in plaque destabilization. Human THP-1 cells were incubated in the presence of CRP at 0 (control group), 25, 50 and 100 mug/mL (CRP groups) for 24 h. In PDTC (a specific NF-kappaB inhibitor) group, the cells were pre-treated with PDTC at 10 mumol/L and then with 100 mug/mL CRP. The conditioned media (CM) and human THP-1 cells in different groups were harvested. MMP-9 expression in CM and human THP-1 cells was measured by ELISA and Western blotting. MMP-9 activity was assessed by fluorogenic substrates. The expression of NF-kappaB inhibitor alpha (IkappaB-alpha) and NF-kappaB P(65) was detected by Western blotting and ELISA respectively. The results showed that CRP increased the expression and activity of MMP-9 in a dose-dependent manner in the human THP-1 cells. Western blotting revealed that IkappaB-alpha expression was decreased in the cells with the concentrations of CRP and ELISA demonstrated that NF-kappaB P65 expression in the CRP-induced cells was increased. After pre-treatment of the cells with PDTC at 10 mumol/L, the decrease in IkappaB-alpha expression and the increase in NF-kappaB P(65) expression in the CRP-induced cells were inhibited, and the expression and activity of MMP-9 were lowered too. It is concluded that increased expression and activity of MMP-9 in CRP-induced human THP-1 cells may be associated with activation of NF-kappaB. Down-regulation of the expression and activity of MMP-9 may be a new treatment alternative for plaque stabilization by inhibiting the NF-kappaB activation.

Percutaneous coronary intervention(PCI) can effectively restore reperfusion of ischemic myocardium in patients with coronary artery disease.But currently PCI treatment is just available for a small proportion of the patients with coronary artery disease,so there was an insufficiency of PCI in patients with coronary artery disease.From the perspective of ethics,the reasons for the phenomenon and some feasible strategies for the problem are also analyzed in this paper.

AIM: To investigate the effects of mechanical stretch under simulated anoxia and reoxygenation conditions on action potential (AP) and effective refractory period (ERP) of calcium preconditioning (CPC) in isolated papillary muscles of guinea pig hearts. METHODS: The intracellular standard glass microelectrode technique was used, and effects of stretch (intensity: 200 mg) on AP and ERP were recorded and observed in CPC papillary muscles. RESULTS: After stretching was implied during anoxia, the reductions of Vmax, RP, APA, APD_(50), ERP and APD_(90) in CPC group were less than those in anoxia-reoxygenation (AR) group, and the CT in CPC group was less elongated. Moreover, after the papillary muscles were stretched during reoxygenated reperfusion, the decreases in Vmax, RP, APA, APD_(50) and ERP in CPC group were less than those in AR group, and the CT and APD_(90) in CPC group were less extended. Streptomycin inhibited the effect of stretch on AP and ERP in CPC group. CONCLUSIONS: Under simulated anoxia and reoxygenation conditions, papillary muscles in CPC group may have better tolerance to the same stretch than those in the AR. Furthermore, streptomycin (a blockade of stretch-activated ionic channels) may inhibit the effect of mechanical stretch on action potential changes in CPC papillary muscles.

n of NF-κ3. Down-regulation of the expression and activity of MMP-9 may be a new treatment alternative for plaque stabilization by inhibiting the NF-κB activation.