论文部分内容阅读
目的:观察红花黄色素对急性心肌缺血大鼠心肌组织中丙二醛(MDA)、超氧化物歧化酶(SOD)的影响及对心肌组织损伤的保护作用。方法:大鼠分为5组,阳性药组(丹参注射液,含生药3.75 g.kg-1)、红花黄色素高、低剂量组(含生药80,40 mg.kg-1)、正常对照组(生理盐水)、模型组(生理盐水),每组13只,均ip,连续7 d,于第8天ip垂体后叶素(Pit)20 U.kg-1造模成大鼠急性心肌缺血模型,测定左心室心肌组织中SOD,MDA的变化以及观察心肌梗死面积的变化。结果:在造模成功的前提下,红花黄色素高、低剂量组与模型组比,可显著增加大鼠左心室心肌中SOD活性[(47.57±11.52)vs(25.97±7.73)U.mg-1,P<0.01;(41.28±11.97)vs(25.97±7.73)U.mg-1,P<0.05],并明显降低MDA含量[(0.29±0.08)vs(1.40±0.26)nmol.mg-1,P<0.01;(0.45±0.15)vs(1.40±0.26)nmol.mg-1,P<0.01],且呈量效关系;经TTC染色,红花黄色素高剂量组梗死区面积明显小于模型组[(32.20±2.2)%vs(43.84±6.3)%,P<0.05]。结论:红花黄色素注射液对Pit所致的急性心肌缺血大鼠有保护作用,其作用机制可能与抗氧化有关。
Objective: To observe the effects of safflor yellow on myocardial malondialdehyde (MDA) and superoxide dismutase (SOD) in myocardial tissue of rats with acute myocardial ischemia and its protective effect on myocardial tissue injury. Methods: The rats were divided into 5 groups: positive group (Salviae miltiorrhizae injection, containing crude drug 3.75 g.kg-1), safflower yellow high and low dose group (containing crude drug 80, 40 mg.kg-1) Control group (saline), model group (saline), each group of 13, ip, for 7 days, on the 8th day pituitary pit (Pit) 20 U.kg-1 modeling acute rat Myocardial ischemia model was used to measure the changes of SOD and MDA in left ventricular myocardium and to observe the change of myocardial infarction area. Results: Compared with the model group, the activity of SOD in the left ventricular myocardium was significantly increased ([(47.57 ± 11.52) vs (25.97 ± 7.73) U.mg (P <0.01); (41.28 ± 11.97) vs (25.97 ± 7.73) U.mg-1, P <0.05] and significantly decreased the content of MDA [(0.29 ± 0.08) vs (1.40 ± 0.26) nmol.mg- 1, P <0.01; (0.45 ± 0.15) vs (1.40 ± 0.26) nmol.mg-1, P <0.01], and showed a dose-effect relationship. The infarct size of high-dose safflor yellow group was significantly smaller The model group [(32.20 ± 2.2)% vs (43.84 ± 6.3)%, P <0.05]. Conclusion: Safflower yellow injection has a protective effect on Pit-induced acute myocardial ischemia in rats, and its mechanism may be related to anti-oxidation.