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Protective Effects of Atorvastatin on Vascular Endothelial Dysfunction Caused by Lysophosphatidyl Choline

Author: LiaoKun
Tutor: YinWeiDong
School: Nanhua University
Course: Pathology and Pathophysiology
Keywords: Atorvastatin Lysophosphatidylcholine Endothelium-dependent relaxation Oxygen radicals Nitric oxide
CLC: R965
Type: Master's thesis
Year: 2011
Downloads: 9
Quote: 0
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Objective: To observe the different doses of atorvastatin statins (atorvastatin, AT) on the protective effect of endothelial dysfunction induced by lysophosphatidylcholine (lysophosphatidyl choline, LPC). Methods: The rabbit isolated vascular rings and cultured human endothelial cell model, the concept of the protective effect of atorvastatin on LPC-induced endothelial dysfunction. Experimental model of isolated thoracic aortic rings were divided into five groups: (1) normal control group; ② The LPC (5 mg / L) injury group; ③ ~ ⑤ LPC (5 mg / L) of atorvastatin (0.05, 0.1 and 0.2 μmol / L ) protection group. Rabbit thoracic aortic ring detect vascular endothelium-dependent relaxation induced by acetylcholine (acetylcholine, ACh) (endothelium-dependent relaxation EDR) and vascular tissue lipid peroxidation metabolism malondialdehyde (malondialdehyde, MDA) content ; vitro hydroponics Cultured human umbilical vein endothelial cells (human umbilical vein of endothelial cells, HUVECs), experimental models, concept Cha Etuo cutting due to the HUVECs oxidative stress impact of statins on the LPC, grouped as follows: ① normal control group; ② L the PC ( 10 mg / L) injury group; the ③ ~~ ⑤ LPC (10 mg / L), atorvastatin statins (0.4 μmol / L, and 2μmol / L, and 10μmol / L) group. Detection of endothelial cell viability, endothelial nitric oxide synthase (of endothelial nitric oxide synthase, eNOS) activity, NO content, oxygen free radicals (ROS). Results: (1) the isolated rabbit thoracic aorta: LPC (5 mg / L), and vascular rings incubated for 15 min, caused a significant reduction in the endothelium-dependent relaxation response, the maximum diastolic ratio than the control group significantly reduced ( P lt; 0.01), atorvastatin dose-dependently reduced the LPC on endothelium-dependent relaxation response to injury, its maximum diastolic ratio than LPC injury group was significantly increased (P lt; 0.01). Non-endothelium-dependent relaxation induced by LPC and atorvastatin sodium nitroprusside had no significant effect. LPC caused by vascular tissue MDA concentrations were significantly increased compared with the control group, there was significant difference (P lt; 0.01); different concentrations of atorvastatin and vascular ring pre-incubation, a dose-dependent reduction of LPC are MDA concentration consistent with LPC injury group significant difference (P lt; 0.01). (2) in cultured human endothelial cells: LPC with HUVECs incubation, lead to reduced cell NO content and eNOS activity, ROS levels; different concentrations of atorvastatin Ting pre-incubation with endothelial cells, a concentration-dependent increase eNOS activity reduce ROS production and NO content. Conclusion: atorvastatin statins exogenous LPC-induced vascular damage of endothelial function have a significant protective effect and its mechanism of action may be against oxidative stress statin atorvastatin.

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