Key result
Amlodipine protects HUVECs from Ang-II-induced endothelial dysfunction and apoptosis by decreasing ROCK1 expression.
Why the study?
The effects and mechanisms of amlodipine therapy on angiotensin-II-induced endothelial dysfunction were not fully understood.
Does amlodipine prevent Ang-II-induced endothelial dysfunction and apoptosis in HUVECs?
Does amlodipine prevent Ang-II-induced endothelial dysfunction and apoptosis in HUVECs?
Amlodipine protects against Ang-II-induced endothelial dysfunction and apoptosis in vitro by downregulating ROCK1 expression.
In vitro findings suggest amlodipine may attenuate Ang-II endothelial injury; leaves open clinical translation and enantiomer preference.
OBJECTIVE: To investigate the effects and mechanisms of amlodipine therapy on endothelium dysfunction induced by angiotensin-II (Ang-II) stimulation. METHODS: Human umbilical vein endothelial cells (HUVECs) were used and divided into five groups: Blank control, Ang-II (10(-6 )mol/L), levorotatory amlodipine (5 × 10(-6 )mol/L) + Ang-II (10(-6 )mol/L), dextrorotatory amlodipine (5 × 10(-6 )mol/L) + Ang-II (10(-6 )mol/L) and racemic amlodipine (5 × 10(-6 )mol/L) + Ang-II (10(-6 )mol/L) groups. Twenty-four hours later, HUVECs were collected for evaluating endothelial nitric oxide synthase (eNOS), p-eNOS, rho-associated kinase 1 (ROCK1), Bcl-2 and Bax expressions. Nitric oxide (NO) concentration within endothelium was also detected. Flow cytometry was conducted to assess HUVECs apoptosis. RESULTS: With 24 hours of Ang-II stimulation, compared to blank control group, expressions of eNOS and p-eNOS and NO production were significantly reduced in Ang-II group (p < 0.05), while adding amlodipine-protected HUVECs from dysfunction induced by Ang-II. In contrast, ROCK1 expression was promoted in Ang-II group (p < 0.05). However, the expression of ROCK1 in each enantiomer of amlodipine group was significantly decreased (p < 0.05). Compared to levorotatory amlodipine group, the magnitude of ROCK1 diminishment in dextrorotatory amlodipine group was more profound (p < 0.05). The pro-survival protein (Bcl-2) was significantly upregulated, while the pro-apoptotic protein (Bax) was significantly downregulated in three amlodipine groups compared to Ang-II group. Flow cytometry revealed that amlodipine therapy could protect HUVECs from apoptosis, and no significant difference between three amlodipine groups was observed. CONCLUSION: Amlodipine could suppress Ang-II-induced endothelial dysfunction and apoptosis through diminishing ROCK1 expression.
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Xu et al. (2015) studied Ang-II-induced endothelium dysfunction. Amlodipine (levorotatory, dextrorotatory, and racemic) vs. Ang-II (10(-6) mol/L) alone and blank control was evaluated on Endothelial dysfunction markers (eNOS, p-eNOS, ROCK1, Bcl-2, Bax expressions, NO concentration, and apoptosis) (p=<0.05). Amlodipine protected HUVECs from Ang-II-induced endothelial dysfunction and apoptosis by significantly decreasing ROCK1 expression (p < 0.05).
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