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首页> 外文期刊>Acta Pharmacologica Sinica >Protective effects of lovastatin on vascular endothelium injured by low density lipoprotein
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Protective effects of lovastatin on vascular endothelium injured by low density lipoprotein

机译：洛伐他汀对低密度脂蛋白损伤血管内皮的保护作用

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AIM: To examine protective effects of lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, on endothelial dysfunction induced by a single intravenous injection of natural low density lipoprotein (n-LDL) and analyze the possible action mechanism of lovastatin. METHODS: Rats were treated by intraperi-toneal injection with lovastatin at dose of 2 or 4 mg/kg body weight once daily for 7 d, and on d 6 a single injection of n-LDL 4 mg/kg was given by sublingual vein. Forty eight hours after injection of n-LDL, the descending thoracic aorta of rats was taken. Acetylcholine (ACh)-induced endothelium-dependent relaxation (EDR) and sodium nitroprusside (SNP)-induced endothelium-independent relaxation of aortic rings were examined in vitro. Malondialdehyde (MDA), nitric oxide (NO), and activity of superoxide dismutase (SOD) as well as level of lipid in serum were analyzed. RESULTS: A single injection of n-LDL inhibited ACh-induced EDR compared with normal control group (maximal relaxation rate: 69.5 %+- 1.2 % vs 91.0 % +- 1.2 %, P<0.05), decreased serum NO level [(7.0 +-0.5) μmol/L vs (11.2 +- 0.9) μmol/L, P<0.05] and serum SOD activity [(371 +- 16) kNU/L vs (405 +- 18) kNU/L, P<0.05] and elevated serum MDA level [(5.4+-0.5) μmol/L vs (3.0+-0.8) μmoyL, P<0.05]. Compared with n-LDL treated group, lovastatin 2 and 4 mg/kg increased EDR( maximal relaxation rate 82.9 % +- 00.5% and 83.7 %+-0.7 % vs 69.5 %+-1.2 %, P<0.05) and elevated NO level [(11.0+-0.7) and (11.2+-0.8) μmol/L vs (7.0+-0.5) μmol/L, P<0.05], increased SOD activity [(402+-15) and (408+-25) kNU/L vs (371+-16) kNU/L, P<0.05], and reduced serum MDA level [(3.3+-0.6) and (3.5+-0.4) μmol/L vs (5.4+-0.5) μmol/L, P<0.05]. But sodium nitroprusside-induced endothelium-independent relaxation and the level of serum lipid in both saline+LDL group and lovastatin-treated group had no marked alteration. CONCLUSION: Lovastatin was able to protect vascular endothelium from dysfunction induced by a single injection of n-LDL.
机译：目的：研究洛伐他汀（一种3-羟基-3-甲基戊二酰辅酶A（HMG-CoA）还原酶的抑制剂）对单次静脉内注射天然低密度脂蛋白（n-LDL）引起的内皮功能障碍的保护作用，并分析洛伐他汀的可能作用机理。方法：大鼠腹腔内注射洛伐他汀，剂量为2或4 mg / kg体重，每天一次，持续7 d，第6天，通过舌下静脉单次注射n-LDL 4 mg / kg。注射n-LDL后四十八小时，取大鼠的降主动脉。体外检查了乙酰胆碱（ACh）诱导的内皮依赖性舒张（EDR）和硝普钠（SNP）诱导的主动脉环非内皮依赖性舒张。分析了丙二醛（MDA），一氧化氮（NO）和超氧化物歧化酶（SOD）的活性以及血清中的脂质水平。结果：与正常对照组相比，单次注射n-LDL可抑制ACh诱导的EDR（最大舒张率：69.5％±1.2％vs 91.0％±1.2％，P <0.05），血清NO水平降低[（7.0 + -0.5）μmol/ L与（11.2 +-0.9）μmol/ L，P <0.05]和血清SOD活性[（371 +-16）kNU / L与（405 +-18）kNU / L，P <0.05 ]和血清MDA水平升高[（5.4 + -0.5）μmol/ L与（3.0 + -0.8）μmoyL，P <0.05]。与n-LDL治疗组相比，洛伐他汀2和4 mg / kg的EDR增加（最大舒张率82.9％+-00.5％和83.7％+-0.7％与69.5％+-1.2％，P <0.05）和NO水平升高[（11.0 + -0.7）和（11.2 + -0.8）μmol/ L与（7.0 + -0.5）μmol/ L，P <0.05]，SOD活性增加[（402 + -15）和（408 + -25） kNU / L vs（371 + -16）kNU / L，P <0.05]，血清MDA水平降低[（3.3 + -0.6）和（3.5 + -0.4）μmol/ L vs（5.4 + -0.5）μmol/ L L，P ＜0.05]。但是在生理盐水+低密度脂蛋白组和洛伐他汀治疗组中，硝普钠诱导的内皮依赖性舒张和血脂水平无明显变化。结论：洛伐他汀能够保护血管内皮免受单次注射n-LDL引起的功能障碍。

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