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1.
China Journal of Chinese Materia Medica ; (24): 2146-2150, 2008.
Article in Chinese | WPRIM | ID: wpr-252179

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effects of tanshinone IIA (TA, one of the active components of Salvia miltiorrhiza Bge), on the proliferation of cultured rat vascular smooth muscle cells (VSMC), and to clarity the probable mechanism.</p><p><b>METHOD</b>Cell culture technique was used in vitro and treated with or without 10% FBS. The inhibitory effect of TA on proliferation of VSMC was observed by cell count, MTU metabolism measuring and BrdU incorporation assay. Flow cytometry was performed to track cell cycle progression. Western bolts were performed to evaluate ERK1/2 activity. The expression of c-fos was examined by RT-PCR.</p><p><b>RESULT</b>The results of cell number, MTU assay and BrdU incorporation showed that TA cound significantly inhibit 10% FBS induced proliferation in a dose-dependent manner. Flow cytometry (FCM) analysis indicated that the G5/G1 phase fraction ratio of TA group was higher than that of 10% FBS group, while the S-phase fraction ratio was lower than that of 10% FBS group. Western blot's results displayed that TA inhibited the phosphorylation of ERK1/2, and in accordance with this findings. TA could decrease the early elevation of c-fos expression.</p><p><b>CONCLUSION</b>These results suggest that TA can inhibit 10% FBS induced the proliferation of VSMC. This effect may be related to its blocking VSMCs cell cycle in G0/G1 phase, inhibiting of the ERK1/2 activity, and decreasing the expression of c-fos.</p>


Subject(s)
Animals , Rats , Aorta , Cell Biology , Cell Cycle , Cell Proliferation , Cells, Cultured , Abietanes , Down-Regulation , Gene Expression , Myocytes, Smooth Muscle , Cell Biology , Phenanthrenes , Pharmacology , Proto-Oncogene Proteins c-fos , Genetics , Metabolism
2.
China Journal of Chinese Materia Medica ; (24): 580-584, 2006.
Article in Chinese | WPRIM | ID: wpr-356763

ABSTRACT

<p><b>OBJECTIVE</b>To observe the preventive and therapeutic effect of tanshinone (TA) on artery restenosis in the rat carotid injury model and explor the mechanism.</p><p><b>METHOD</b>Male SD rats were randomly divided into model control group, and low dose, moderate dose and high dose TA groups. Each group had 10 rats. The rats in the high, moderate and low dose groups were respectively fed with TA 120, 40,13.3 mg x kg(-1) x d(-1) by gast rogavage; the rats in the model control group were fed with the same volume solvent. Two days later, the rat's right carotid artery was injuried by balloon dilatation to induce intimal thickening for establishing the restenosis model. After 2 weeks of treatment, the artery was harvested and stained by hematoxylin-elsin (HE) and immunohistochemistry of PCNA, NF-kappaB and iNOS. The morphological changes were checked under microscope. The area of the intimal and medial layer of the vessels, and their ratios were analyzed with image analysis software. The expression level of PCNA, NF-kappaB and iNOS were used as the positive index.</p><p><b>RESULT</b>The intimal area and intima-to-media ratio of the injuried artery increased obviously, suggesting the model was successful. Compared with the model group, TA significantly decreased the intimal area and intima-to-media ratio (P < 0.05), and also decreased the positive index of PCNA and the positive ratio of NF-kappaB and iNOS (P < 0.05).</p><p><b>CONCLUSION</b>TA can effectively inhibit intimal thickening and inflammation. This result suggestes that TA may play a positive role in the prevention of restenosis after PTCA.</p>


Subject(s)
Animals , Male , Rats , Angioplasty, Balloon, Coronary , Carotid Artery Injuries , Carotid Artery, Common , Metabolism , Pathology , Carotid Stenosis , Metabolism , Pathology , Abietanes , NF-kappa B , Metabolism , Nitric Oxide Synthase Type II , Metabolism , Phenanthrenes , Pharmacology , Plants, Medicinal , Chemistry , Proliferating Cell Nuclear Antigen , Metabolism , Random Allocation , Rats, Sprague-Dawley , Salvia miltiorrhiza , Chemistry , Tunica Intima , Metabolism , Pathology
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