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. 2019 Feb 25;10:142. doi: 10.3389/fphar.2019.00142

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Copyright © 2019 Ji, Ge, Xu, Ye, Fan, Zhang, Mei, Zhang, Ying, Yang and Li.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Vildagliptin inhibited ligation injury-induced proliferation and hypertrophy in VSMCs. (A) Representative expressions of PCNA, Cyclin D and CDK2 (indices of proliferation) analyzed by Western-blot. (B) Representative expression of α-SMA (an index of hypertrophy) analyzed by Western-blot. (C). Quantification data of PCNA, Cyclin D1, CDK2, and α-SMA were determined by calculating the ratio of the intensity of the signal for the protein of interest to that of the normalization control. GAPDH served as the loading control. The value from the sham carotid artery treated with PBS was considered as 100% (control). Bars represented the ratio of the quantitative data from experimental groups to that from the control group. ^∗P < 0.05 vs. sham, ^#P < 0.05 vs. injured carotid artery (n = 3).