PTS预处理对大鼠心肌缺血再灌注损伤保护效果及机制研究

目的探讨人参三醇皂苷(PTS)预处理对大鼠心肌缺血再灌注损伤(MIRI)的保护作用机制。方法选用Wistar大鼠作为研究对象,随机分组:假手术组(生理盐水2 m L/kg体质量)、模型组(生理盐水2 m L/kg体质量)、PTS低剂量组(25 mg/kg)、PTS中剂量组(45 mg/kg)、PTS高剂量组(90 mg/kg)、阳性药组(生脉注射液450 mg/kg)。连续7 d腹腔注射给药,于末次给药1 h后进行MIRI造模手术,再灌注24 h后取材料测定各项指标。监测大鼠心电图ST段变化;检测血清肌酸激酶同工酶(CK-MB)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)水平;采用PCR检测心肌组织Bcl-2和Bax mRNA表达水平;光镜和电镜观察心肌组织病理和心肌细胞超微结构的改变。结果与模型组比较,PTS中剂量组和高剂量组能显著降低MIRI模型大鼠ST段和血清CK-MB、IL-6、TNF-α水平,改善心肌结构的损伤程度,增加抗凋亡蛋白Bcl-2表达,抑制前凋亡蛋白Bax的表达。结论PTS对MIRI大鼠心肌具有保护作用,其作用机制可能是通过抑制炎症因子表达和调节凋亡关键酶来实现。

Protective Effect and Mechanism of PTS Preconditioning on Myocardial Ischemia-reperfusion Injury in Rats

Objective To investigate the protective mechanism of ginseng triolsaponin ( PTS) preconditioning on myocardial ischemia-reperfusion injury ( MIRI) in rats. Method After one week of adaptive feeding, 120Wister rats were randomly divided into a sham operation group ( normal saline 2 mL/kg) , a model group ( normal saline 2 mL/kg) , a PTS low dose group ( 25 mg/kg) , and a PTS medium dose group. (45 mg/kg) , PTS high dose group (90 mg/kg) , positive drug group ( shengmai injection 450 mg/kg) .The drug was administered intraperitoneally for 7 consecutive days. MIRI modeling was performed 1 hour after the last administration , and the materials were measured after 24 hours of reperfusion. Monitoring ST segment changes of rat electrocardiogram ； detecting serum creatine kinase isoenzyme ( CK-MB) , interleukin-6 (IL-6) and tumor necrosis factor-— ( TNF-—) levels; detecting myocardial tissue by PCR Bcl-2 and Bax mRNA expression levels ; myocardial histopathology and ultrastructural changes of cardiomyocytes were observed by light and electron microscopy. Result Compared with the model group , the PTS medium dose group and the high dose group can significantly reduce the STsegmentand serum CK- MB, IL-6, TNF-— levels in the MIRI model rats, improve the damage of myocardial structure, and increase the anti-apoptotic protein Bcl-2 expression inhibits the expression of the proapoptotic protein Bax. Conclusion PTS has protective effects on MIRI rat myocardium , and its mechanism maybe achieved by inhibiting the expression of inflammatory factors and regulating keyenzymes of apoptosis.