解毒活血方含药血清对氧化低密度脂蛋白损伤血管内皮细胞及细胞间黏附分子1的影响

Serum prepared with detoxication-promoting blood flow recipe on vascular endothelium cell and intercellular adhesion molecule-1 injured by oxidized low density lipoprotein

目的通过观察解毒活血方含药血清(SPR)对氧化低密度脂蛋白(ox-LDL)损伤内皮细胞及细胞间黏附因子1(ICAM-1)的影响,探讨该方防治冠心病的作用机制。方法用10只Wistar大鼠,分成两组,每组5只,分别制备空白血清和解毒活血方含药血清,然后依据细胞培养条件对提取的血清进行分组。①空白对照组:20%空白血清+5%新生牛血清(FCS)培养液;②病理模型组:20%空白血清+100mg/L ox-LDL+5%FCS培养液;③SPR低剂量组:10%SPR+10%空白血清+100mg/L ox-LDL+5%FCS培养液;④SPR高剂量组:20%SPR+100mg/L ox-LDL+5%FCS培养液,每组各6个标本,共获得24个标本,分别检测各组超氧化物歧化酶(SOD)、丙二醛(MDA)、ICAM-1等指标的变化。结果病理模型组SOD比空白对照组明显降低,加入SPR后有明显提高,SPR高剂量组比SPR低剂量组提高更多(P<0.05或<0.01),分别为(58.26±1.34)kU/L vs(65.10±1.35)kU/L,(63.57±1.63)kU/L,(67.63±2.95)kU/L。病理模型组MDA水平和ICAM-1表达与空白对照组比较明显增加,加入SPR后有明显降低,SPR高剂量组比SPR低剂量组降低更多,分别为MDA(10.02±1.66)μmol/L vs(6.68±0.82)μmol/L,(6.87±1.26)mg/L,(6.83±0.46)mg/L;ICAM-1(0.51±0.06)mg/L vs(0.37±0.05)mg/L,(0.45±0.02)mg/L,(0.40±0.04)mg/L。结论 SPR防治冠心病的机制与抗脂质过氧化、抑制或减少炎症因子ICAM-1的释放有关。

Objective The aim was to explore the mechanism of the serum prepared with detoxication-promoting blood flow recipe（SPR） in prevention of coronary heart disease, we observed the effects of this recipe on the vascular endothelium cell and intercellular adhesion molecule-1 （ICAM-1） both injured by oxidized low density lipoprotein（ox-LDL）. Methods Ten Wistar rats were divided into two groups,each group five rats,then the control serum and the recipe serum were prepared. According different conditions for cell culture from the serum, four groups were established,including： ① control group 20% control serum ＋ 5% culture fluid from fetal cow serum （FCS）; ② pathological model group 20% control serum＋ 100 mg/L ox-LDL＋5 % culture fluid from FCS;③SPR lowe-dose 10% SPR＋ 10 % control serum＋ 100 mg/L ox-LDL＋ 5% culture fluid from FCS;④SPR high-dose 20 % SPR＋ 100 mg/L ox-LDL＋ 5% culture fluid from FCS, each group contained six specimens, altogether 24 specimens. Finally, the variation indexes of superoxide dismutase（SOD）,malondialdehyde（MDA）,ICAM-1 were detected. Results Compared to that of control group, the activity of SOD in pathological model group decreased significantly, it improved by adding SPR, also the effect was much higher in high-dose group than in low-dose group （ P 〈 0.05 or 〈 0.01 ）, respectively （58.26±1.34） kU/L vs （65.10±1.35） kU/L,（63. 57±1. 63） kU/L,（67. 634±2.95） kU/L. The levels of MDA and ICAM-1 in pathological model group, comparing to those of control group, were dramatically increased, however, the levels decreased distinctly with SPR infusion and the levels in high-dose group were much lower than those in low-dose group,MDA respectively （10.02±1.66） μmol/L vs （6.68±0. 82） μmol/L, （6.87±1.26） mg/L, （6.83±0.46） mg/L;ICAM-1（0. 51±0. 06） mg/L vs （0.37±0.05） mg/L,（0.45±0.02） mg/L,（0.40±0.04） mg/L. Conclusion The mechanisms of the recipe that prevent and treat the coronary heart disease are related to the anti-lipid peroxide and the depressing-or-decreasing release of inflammatory faction ICAM-1.