Breviscapine inhibits high glucose-induced proliferation and migration of cultured vascular smooth muscle cells of rats via suppressing the ERK1/2 MAPK signaling pathway
Abstract
Aim: To investigate the influences of breviscapine, a flavonoid extracted from Erigeron breviscapus, on the proliferation and migration of vascular smooth muscle cells (VSMCs) cultured in a high glucose medium and the underlying mechanisms.
Methods: VSMCs were isolated from thoracic aortas of male Sprague-Dawley rats and cultured in vitro. Cell proliferation was evaluated using Counting Kit-8 cell viability assay. Cell migration was evaluated using transwell migration assay and in vitro scratch assay. The expression and activity of protein kinase C-β2 (PKC-β2), extracellular signal-regulated kinase 1/2 (ERK1/2), p38 mitogen-activated protein kinase (p38), and JNK mitogen-activated protein kinase (JNK) were measured with Western blotting.
Results: Exposure of VSMCs to a high glucose (25 mmol/L) medium significantly increased the proliferation and migration potential as compared to the control group. Pretreatment with breviscapine (65 μmol/L and 108 μmol/L) attenuated high glucose-enhanced proliferation and migration of VSMCs. Exposure of VSMCs to the high glucose medium activated both the PKC-β2 and ERK1/2 MAPK, but not the p38 and JNK MAPK. Pretreatment with breviscapine (65 μmol/L and 108 μmol/L) blocked high glucose-induced increase of the ERK1/2 activity, but not that of the PKC-β2 activity.
Conclusion: Our study demonstrated that breviscapine ameliorates high glucose-induced proliferation and migration of VSMCs via inhibiting ERK1/2 MAPK signaling.
Keywords:
Methods: VSMCs were isolated from thoracic aortas of male Sprague-Dawley rats and cultured in vitro. Cell proliferation was evaluated using Counting Kit-8 cell viability assay. Cell migration was evaluated using transwell migration assay and in vitro scratch assay. The expression and activity of protein kinase C-β2 (PKC-β2), extracellular signal-regulated kinase 1/2 (ERK1/2), p38 mitogen-activated protein kinase (p38), and JNK mitogen-activated protein kinase (JNK) were measured with Western blotting.
Results: Exposure of VSMCs to a high glucose (25 mmol/L) medium significantly increased the proliferation and migration potential as compared to the control group. Pretreatment with breviscapine (65 μmol/L and 108 μmol/L) attenuated high glucose-enhanced proliferation and migration of VSMCs. Exposure of VSMCs to the high glucose medium activated both the PKC-β2 and ERK1/2 MAPK, but not the p38 and JNK MAPK. Pretreatment with breviscapine (65 μmol/L and 108 μmol/L) blocked high glucose-induced increase of the ERK1/2 activity, but not that of the PKC-β2 activity.
Conclusion: Our study demonstrated that breviscapine ameliorates high glucose-induced proliferation and migration of VSMCs via inhibiting ERK1/2 MAPK signaling.