Key result
Stigmasterol inhibits vascular smooth muscle cell proliferation by arresting cell cycle and decreasing ROS.
Why the study?
Excessive proliferation of vascular smooth muscle cells contributes to cardiovascular diseases such as atherosclerosis and restenosis, and effective inhibitors are needed.
Does stigmasterol prevent vascular cell proliferation in A7r5 aortic smooth muscle cells stimulated by Ang II?
Does stigmasterol prevent vascular cell proliferation in A7r5 aortic smooth muscle cells stimulated by Ang II?
Stigmasterol inhibits Ang II-induced proliferation of vascular smooth muscle cells, suggesting potential therapeutic value against atherosclerosis and restenosis.
Hypothesis-generating for stigmasterol in vascular disease; leaves open any therapeutic role in atherosclerosis or restenosis.
Excessive proliferation of vascular smooth muscle cells is a crucial event in the pathogenesis of several cardiovascular diseases, including atherosclerosis and restenosis. In this study, we reported that stigmasterol was effective in inhibiting vascular cell proliferation exemplified by using A7r5 cells stimulated by Ang II. Mechanism analysis showed that this inhibiting effect mainly occurred by the arrest of the cell-cycle and promotion of apoptosis. In addition, stigmasterol inhibition effects were detected in association with decreased ROS production, enhanced SOD and CAT activity, decreased abundance of cyclin A, CDK2, PCNA, bax and bcl-2, and increased levels of p53 protein. Our study provided implications for the development of therapeutic strategies to protect against certain cardiovascular pathologies, such as atherosclerosis and restenosis.
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Li et al. (2015) studied Vascular smooth muscle cell proliferation. Stigmasterol was evaluated on Vascular cell proliferation. Stigmasterol effectively inhibited Ang II-induced proliferation of A7r5 vascular smooth muscle cells by arresting the cell cycle, promoting apoptosis, and decreasing ROS production.
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