摘要
Background Dicycloplatin is a relatively safe third generation focused on the effects of dicycloplatin on in vitro proliferation （HASMC） and human aortic endothelial cells （HAEC）. platinum-complex anti-cancer drug. The present study and apoptosis of human aortic smooth muscle cells Methods Proliferation of HASMC and HAEC, DNA content, and cellular levels of proliferation- and apoptosis-related proteins were assessed using the （3-（4,5-dimethylthiazol-2-yl）-5-（3-carboxymethoxyphenyl）-2-（4-sulfophenyl）- 2H-tetrazolium） （MTS） assay, flow cytometry and Western blotting assays, respectively. Results Dicycloplatin at 10 ng/ml significantly inhibited HASMC proliferation, however, 10 μg/ml were required to significantly inhibit HAEC proliferation. Cell cycle analysis showed that dicycloplatin was a non-specific inhibitor of the cell cycle. Although dicycloplatin significantly decreased proliferating cell nuclear antigen （PCNA） expression in HASMC at all concentrations tested, it did not significantly affect PCNA expression in HAEC; Bax and p53 protein expression was upregulated in dicycloplatin groups. Conclusions Dicycloplatin at nanogram concentrations significantly inhibits HASMC proliferation, although the effect is relatively weaker than that of sirolimus. In contrast, the effect of dicycloplatin on inhibition of HAEC proliferation is much less pronounced than that on HASMC. The latter characteristics point to the potential for use of dicycloplatin in drug-eluting stents.
Background Dicycloplatin is a relatively safe third generation focused on the effects of dicycloplatin on in vitro proliferation （HASMC） and human aortic endothelial cells （HAEC）. platinum-complex anti-cancer drug. The present study and apoptosis of human aortic smooth muscle cells Methods Proliferation of HASMC and HAEC, DNA content, and cellular levels of proliferation- and apoptosis-related proteins were assessed using the （3-（4,5-dimethylthiazol-2-yl）-5-（3-carboxymethoxyphenyl）-2-（4-sulfophenyl）- 2H-tetrazolium） （MTS） assay, flow cytometry and Western blotting assays, respectively. Results Dicycloplatin at 10 ng/ml significantly inhibited HASMC proliferation, however, 10 μg/ml were required to significantly inhibit HAEC proliferation. Cell cycle analysis showed that dicycloplatin was a non-specific inhibitor of the cell cycle. Although dicycloplatin significantly decreased proliferating cell nuclear antigen （PCNA） expression in HASMC at all concentrations tested, it did not significantly affect PCNA expression in HAEC; Bax and p53 protein expression was upregulated in dicycloplatin groups. Conclusions Dicycloplatin at nanogram concentrations significantly inhibits HASMC proliferation, although the effect is relatively weaker than that of sirolimus. In contrast, the effect of dicycloplatin on inhibition of HAEC proliferation is much less pronounced than that on HASMC. The latter characteristics point to the potential for use of dicycloplatin in drug-eluting stents.
