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肝细胞生长因子治疗大鼠冠状动脉粥样硬化的作用及机制 被引量:2

The protective role of hepatocyte growth factor in experimental atherosclerosis rats
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摘要 目的 探讨肝细胞生长因子(HGF)对大鼠冠状动脉粥样硬化(AS)的保护作用及其机制.方法 SD大鼠50只,采用连续饲喂高脂饲料12周联合一次性腹腔注射维生素D3的方法建立大鼠AS模型,按照随机数字表法分为5组,正常组、模型组和HGF低剂量组、HGF中剂量组、HGF高剂量组,每组各10只.经过12周的饲养后,处死大鼠,分别进行主动脉血管形态检测、血清中甘油三酯(TG)、高密度脂蛋白(HDL)、氧化低密度脂蛋白(oxLDL)、丙二醛(MDA)和超氧化物歧化酶(SOD)水平测定.结果 高脂饲养12周后,HGF治疗组可以显著减轻血管损伤;HGF中、高剂量治疗组大鼠TG水平分别为(1.197 ±1.107)和(0.972 ±0.104) nmol/L,显著低于模型组[(1.842±0.228) nmol/L,P<0.05];HGF中、高剂量治疗组大鼠HDL水平分别为(0.478 ±0.081)和(0.610±0.101) nmol/L,显著高于模型组[(0.332 ±0.047) nmol/L,P<0.05];HGF中、高剂量治疗组大鼠血清oxLDL水平为(31.21 ±9.21)和(23.29±5.66) ng/dl,显著低于模型组[(59.27±10.24) ng/dl,P<0.05,P<0.01];HGF中、高剂量治疗组大鼠血清MDA水平为(8.670±1.097)和(7.220±1.144) nmol/L,显著低于模型组[(11.390±2.447) nmol/L,P<0.05];HGF高剂量治疗组大鼠血清SOD水平为(134.10±19.27) U/ml,显著高于模型组[(84.23±12.04) U/ml,P<0.05].结论 HGF可以减轻AS大鼠主动脉病理损伤,调节AS大鼠血脂紊乱,降低AS大鼠血清MDA、oxLDL水平、升高SOD水平,对大鼠AS具有保护作用. Objective To investigate the protective role of hepatocyte growth factor (HGF) in experimental atherosclerosis (AS) rats and its mechanisms.Methods Rat AS model was established by high lipid feed for consecutive 12 weeks and received intraperitoneal injection of vitamin D3 one time.Fifty SD rats were randomly divided into 5 groups by random number table:normal group,model group,and HGF low-,medium-and high-dosage treatment groups (n =10 each).The injury of arteries,triglycerides (TG),high density lipoprotein (HDL),oxidized low density lipoprotein (oxLDL),malondialdehyde (MDA) and superoxide dismutase (SOD) levels in serum were measured after 12 weeks.Results After 12 weeks,the injury of arteries in HGF treatment group was milder than that of model group.The TG levels in medium-and high-dosage HGF treatment groups [(1.197 ± 1.107),and (0.972 ± 0.104) nmol/L,respectively] were significantly lower than those of model group [(1.842 ± 0.228) nmol/L,P < 0.05,P < 0.01,respectively].The HDL levels of medium-and high-dosage HGF treatment groups [(0.478 ± 0.081) nmol/L,and (0.610 ±0.101) nmol/L,respectively] were significantly higher than those of model group [(0.332 ± 0.047) nmol/L,P < 0.05,P < 0.01,respectively].The oxLDL levels in medium-and high-dosage HGF treatment groups [(31.21 ± 9.21) ng/dl,and (23.29 ± 5.66) ng/dl,respectively] were significantly lower than those of model group [(59.27 ± 10.24) ng/dl,P <0.05,P <0.01,respectively].The MDA levels in medium-and high-dosage HGF treatment groups [(8.67 ± 1.097) nmol/L,and (7.22 ± 1.144) nmol/L,respectively] were significantly lower than those of model group [(11.39 ± 2.447) nmol/L,P < 0.05,P < 0.01,respectively].The SOD levels in high-dosage HGF treatment group [(134.10 ± 19.27) U/ml] was significantly higher than those of model group [(84.23 ± 12.04) U/ml,P < 0.05].Conclusion HGF has a protective effect on AS by attenuating the arteries injury,regulating the disorder of blood lipids,decreasing MDA and oxLDL levels,and increasing SOD level.
出处 《中华实验外科杂志》 CAS CSCD 北大核心 2015年第7期1613-1615,共3页 Chinese Journal of Experimental Surgery
关键词 动脉粥样硬化 肝细胞生长因子 血脂 氧化应激 Atherosclerosis Hepatocyte growth factor Blood lipids Oxidative stress
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