Effects of Atorvastatin on Tumor Necrosis Factor-α Induced Endothelial Lipase Secreting by Rat Vascular Smooth Muscle Cell
Bian Yun
Abstract
Bian Yun
Abstract
Aim To investigate the effects of atorvastatin on TNF-α induced endothelial lipase secreting by rat vascular smooth muscle cells. Methods The rat vascular smooth muscle cells were obtained from thoracic aortas and cultured by tissue explant method. Rat vascular smooth muscle cells were first incubated in serum-free medium with 50 μg/Ltumor necrotic factor-alpha; 1 hour later,atorvastatins with different concentration(1×10-7 mmol/L ,1×10-6mmol /L,1×10-5 mmol/L)were added to the medium. 24 hours later, cells of different groups were collected and endothelial lipase mRNA levels were determined by reverse transcription-polymerase chain reaction. In another group with atorvastatin concentration of 1×10-5 mmol/L, endothelial lipase levels were respectively determined after 6. 12 and 24 hours. Results Endothelial lipase expressions of atorvastatin intervent groups(1×10-7 mmol/L ,1×10-6 mmol /L,1×10-5 mmol/L) decreased significantly vs TNF-α group(P0.05). The levels of endothelial lipase expression decreased initially with the atorvastatin concentration raise(P0.05). Endothelial lipase expressions of atorvastatin time-intervent groups(6,12,24 h) decreased significantly vs. TNF-α group(P0.05). The levels of endothelial lipase expression decreased initially with the time extended (P0.05). Conclusions Atorvastatin can inhibit endothelial lipase mRNA secreting by tumor necrotic factor-alpha stimulated vascular smooth muscle cells, in a concentration-time dependent manner.
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Aim To investigate the effects of atorvastatin on TNF-α induced endothelial lipase secreting by rat vascular smooth muscle cells. Methods The rat vascular smooth muscle cells were obtained from thoracic aortas and cultured by tissue explant method. Rat vascular smooth muscle cells were first incubated in serum-free medium with 50 μg/Ltumor necrotic factor-alpha; 1 hour later,atorvastatins with different concentration(1×10-7 mmol/L ,1×10-6mmol /L,1×10-5 mmol/L)were added to the medium. 24 hours later, cells of different groups were collected and endothelial lipase mRNA levels were determined by reverse transcription-polymerase chain reaction. In another group with atorvastatin concentration of 1×10-5 mmol/L, endothelial lipase levels were respectively determined after 6. 12 and 24 hours. Results Endothelial lipase expressions of atorvastatin intervent groups(1×10-7 mmol/L ,1×10-6 mmol /L,1×10-5 mmol/L) decreased significantly vs TNF-α group(P0.05). The levels of endothelial lipase expression decreased initially with the atorvastatin concentration raise(P0.05). Endothelial lipase expressions of atorvastatin time-intervent groups(6,12,24 h) decreased significantly vs. TNF-α group(P0.05). The levels of endothelial lipase expression decreased initially with the time extended (P0.05). Conclusions Atorvastatin can inhibit endothelial lipase mRNA secreting by tumor necrotic factor-alpha stimulated vascular smooth muscle cells, in a concentration-time dependent manner.
Key concepts: Lipase, Atorvastatin, Vascular smooth muscle, Internal medicine, Endocrinology, Tumor necrosis factor alpha, Endothelial stem cell, Lipoprotein lipase