目的探讨硫辛酸(LA)对急性冠脉综合征(ACS)患者的心肌保护作用及可能机制。方法选择ACS患者63例,分为硫辛酸组33例和常规药物组30例,硫辛酸组给予常规药物+硫辛酸治疗,常规药物组给予常规药物治疗,疗程1周。用药前(0 h)、24 h、1周抽取空腹静脉血,分别通过比色法、双抗体夹心ABC-ELISA法和免疫散色比浊法测定乙醛脱氢酶2(ALDH2)活性、8-异前列腺素F2a(8-iso PGF2a)及高敏C反应蛋白(hs-CRP)含量并进行分析。结果治疗24 h后,两组患者ALDH2活性水平显著上升(P〈0.001),8-iso PGF2a含量显著下降(P〈0.001);硫辛酸组ALDH2活性升高(P〈0.01),8-iso PGF2a含量下降较常规药物组更为明显(P〈0.05);治疗1周后,两组ALDH2活性水平较0 h明显上升(P〈0.001),8-iso PGF2a含量较0 h、24 h均显著下降(P〈0.001),hs-CRP含量较0 h明显下降(P〈0.001),硫辛酸组ALDH2活性、8-iso PGF2a、hs-CRP含量的变化较常规药物组更为明显(P〈0.05)。结论硫辛酸可以通过上调ALDH2活性、下调8-iso-PGF2a、hs-CRP的含量,抑制氧化应激及炎症反应而产生心肌保护作用。
Objective To investigate whether lipoic acid can protect the myocardium of patients with acute coronary syndrome and explore the mechanism.Methods 63 patients with acute coronary syndrome were randomly divided into two groups: the lipoic acid group and the conventional medicine group.Patients in the lipoic acid group were given 600 mg lipoic acid every day,while patients in the conventional medicine group were given routine drugs.The course of treatment was one week.The activity of ALDH2,concentrations of hs-CRP and 8-iso PGF2a in all patients were examined before,24 hours and 1 week after the medication.Results After24-hour treatment,the activity of ALDH2 in the two groups were significantly higher than before(P〈0.001),while the concentration of 8-iso PGF2a decreased(P〈0.001).The activity of ALDH2 in the lipoic acid group was much higher than in the conventional medicine group(P〈0.01),and 8-iso PGF2a in the lipoic acid group was significantly lower than in the conventional medicine group(P〈0.05).After 1week,compared to the before-medication data,the activity of ALDH2 in the two groups was significantly higher(P〈0.001),and the concentration of 8-iso PGF2a and hs-CRP were lower(P〈0.001).The variation of these three parameters in the lipoic acid group was larger than the conventional medicine group.Also,concentration of 8-isoPGF2a after one-week treatment was lower than that at the end of 24-hour treatment.Conclusion Lipoic acid may increase the activity of antioxidant enzymes and reduce the serum level of oxidative stress and inflammation factors to protect the myocardium of patients with acute coronary syndrome.