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@#【Objective】To observe whether berberine can inhibit vascular smooth muscle cells（VSMC）proliferation induced by mechanical strength stress and to investigate the role of MAPK pathway in it.【Methods】The cultured VSMC were divided into 4 groups：negative control group（NC group），stretch stress group（SS group），berberine pretreated and stretch stress stimulation group（BBR+SS group），and berberine group. In NC group，phosphate buffer saline was used as a negative control；in SS group，stretch stress was given to VSMC；in BBR+SS group，VSMC were pretreated with berberine for 1 hour and then exposed to stretch stress；in BBR group，VSMC were treated only with berberine for 1 hour and cultured in serum- free DMEM afterwards. We collected VSMC in each group ，detected and analyzed their MAPK phosphorylation，proliferation and migration by using Western blotting，immunofluorescence and wound-healing assay respectively. 【Results】 Compare with NC group，stretch stress markedly induced VSMC proliferation and migration ，which could be inhibited significantly by berberine. Stretch stress obviously increased phosphorylation of MAPK （ERK，JNK，p38），which could be inhibited by berberine in a concentration dependent manner. 【Conclusion】 Berberine inhibits hypertension-induced proliferation and migration of VSMC through MAPK pathway. The results revealed the new use and mechanism of berberine，and provided important data for further study on the prevention and treatment of vascular remodeling caused by abnormal increase of mechanical stress in hypertension.
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Aim: To observe the effect of ursolic acid(UA)on the proliferation of rat vascular smooth muscle cell(VSMC)induced by high-level glucose and explore its relationship with p38MAPK signal transduction pathway.Methods: The proliferation of VSMC induced by high-level glucose(25 mmol/L glucose)was adopted as model,the inhibition of UA on the proliferation of VSMC was measured by MTT assay,and the expression lev-els of phospho-p38MAPK was detected by cell-based ELISA as well as the expression of c-fos protein was exam-ined by SABC method.Results: UA(20 μmol/L and 40 μmoL/L)inhibited glucose-induced proliferation of VSMC(P <0.05).Compared with the group subjected to glucose induction,UA decreased the expression levels of phosphorylated p38MAPK(P < 0.05),and also inhibited c-fos expression.Conclusion: UA suppressed glucose induced proliferation of VSMC,which might be related to the suppression of the activation of p38MAPK signal transduction pathway,and thereby down-regulated c-fos expression.
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Objective To observe the vascular collagen remodeling, apoptosis and Bcl-2/Bax of vascular smooth muscle cells in carotid artery on SHR . Methods 12 SHR treated with Irbesartan ,12 SHR without treated Irbesartan ,12 wistar rats were normotensive control group. The vascular volume fraction of Collagen were determined by picrosirius red staining .The expression of the proteins Bcl-2 and Bax were determined by Immunhistochemia,VSMC apoptosis was identified by in situ TDT-mediated dUTP nick end labeling(TUNEL). Results Significant Fibrosis exists in carotid artery of SHR. After 20 week's treating, the vascular volume fraction of Collagen and the ratio of wall/cavity were descended, but weren't parallel. The expression of the protein Bcl-2 and APOI were higher than the subjects of normotensive control, its reduced after treating; The expression of the proteins Bax was similar with control, it increased after treating. Conclusions The results suggest that vascular collagen remodeling exist, its maybe related with apoptosis , the proteins Bcl-2 and Bax of VSMC. The Irbesartan can treat it.
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By means of 3H-Thymidine and3H-Leucine incorporation, we observed that CGRP inhibited the multiplication of SHR's aortic smooth muscle cells (VSMCs) and the proliferation of VSMCs stimulated by Endothelin. These results suggest that CGRP may be a natu-ral antagonist of Endothelin in human body.