梓醇减轻心肌缺血/再灌注损伤及机制

目的:观察梓醇是否可减轻急性心肌缺血/再灌注（MI/R）损伤。方法:建立大鼠MI/R模型，随机给予生理盐水和梓醇预处理，全程检测大鼠的心脏功能。再灌注末检测大鼠心肌梗死(MI)面积、心肌细胞凋亡指数、血清肌酸激酶和乳酸脱氢酶的活性、心肌组织过氧亚硝基阴离子（ONOO-）、一氧化氮（NO）、超氧化物及超氧化物歧化酶（SOD）的含量。结果:梓醇预处理可明显改善心脏功能，减少心肌梗死面积和心肌细胞的凋亡与坏死（均P<0.05）。同时，ONOO-和超氧化物的产生也显著减少（P<0.05）；NO和SOD的含量显著增加（均P<0.05）。缺血前给予ONOO-清除剂尿酸（UA）显著减少ONOO-生成及MI范围（P<0.05），但不能额外增强梓醇降低ONOO-及减小MI范围的效应（MI/R+梓醇+UA组 vs. MI/R+梓醇组）。结论:梓醇可抑制ONOO-形成，从而减轻MI/R损伤，其机制可能与增加NO水平及减少超氧化物生成有关。

Cardioprotective effects of catalpol against ischemia/reperfusion insult

AIM:To investigate the cardioprotective effect of catalpol in acute myocardial ischemia/reperfusion (MI/R). METHODS: Adult male rats were subjected to 30 min of myocardial ischemia and 3 h of reperfusion and were treated with saline or catalpol (5 mg/kg, i.p., 5 min before reperfusion). Left ventricle systolic pressure (LVSP) and the maximal first derivative of developed pressure (±LV dP/dtmax) were monitored throughout the experiments. Myocardial infarction size, serum creatine kinase (CK) activity, lactate dehydrogenase (LDH) activity, apoptosis index, caspase-3 activity, nitric oxide (NO), superoxide dismutase (SOD), superoxide and peroxynitrite (ONOO-) production were determined at the end of reperfusion. RESULTS: Compared with sham, pretreatment with catalpol significantly improved cardiac functions and reduced myocardial infarction, apoptosis and necrosis of cardiomyocytes after MI/R (all P<0.05). Meanwhile, ONOO- formation was markedly reduced after catalpol treatment (3.01±0.22 vs. 4.66±0.53 pmol/mg protein in vehicle, P<0.05). Catalpol increased NO production and anti-oxidant capacity and reduced MI/R-induced superoxide anion (·O-2) production in I/R hearts. In addition, treatment with the potent ONOO- scavenger uric acid (UA) significantly decreased ONOO- production and protected myocardium against MI/R injury, whereas the same treatment with UA could not further enhance cardioprotective effects of catalpol (P>0.05 vs. catalpol alone). CONCLUSION: Catalpol provides cardioprotection against MI/R insult by attenuating ONOO- formation, which is attributable to the increased NO production and decreased ·O-2 production.