不同黄芪剂量补阳还五汤促进大鼠慢性难愈性创面修复愈合的实验研究

目的：观察不同黄芪剂量补阳还五汤治疗大鼠慢性难愈性创面的疗效,探讨黄芪剂量对补阳还五汤疗效的影响。方法：在53只雄性sD大鼠背部制造全层皮肤缺损开放性创面,除正常对照组外,大鼠肌肉注射醋酸氢化可的松建立难愈性创面模型,随机分为模型组,黄芪15g、30g、60g、120g补阳还五汤组（以下简称黄芪15g、30g、60g、120g组）,观察各组大鼠创面愈合率、愈合时间。结果：模型组与正常对照组比较,创面愈合率低,愈合时间延长（P〈0．01,P〈0．05）;不同黄芪剂量补阳还五汤各组与模型组比较,创面愈合率显著提高,愈合时间明显缩短（P〈0．01,P〈0．05）,与正常对照组比较,差异无统计学意义（P〉0．05）;黄芪120g组创面愈合率高于黄芪15g组（P〈0．01,P〈0．05）,愈合时间短于后者（P〈0．05）,与黄芪30g、60g组比较差异无统计学意义（P〉0．05）。结论：不同黄芪剂量补阳还五汤均可明显促进慢性难愈性创面的修复愈合,以黄芪30、60、120g的补阳还五汤的疗效更佳。     

冠心康对大鼠缺血心肌细胞ATP敏感钾通道亚基Kir6.1、Kir6.2、SUR2A和SUR2B表达的影响

目的：通过观察中药复方冠心康对大鼠缺血心肌细胞ATP敏感钾（ATP-sensitive potassium,K_（ATP））通道亚基的影响,探讨冠心康保护心血管、抗心肌缺血的可能作用机制。方法：48只SPF级Wistar大鼠随机分为正常组、模型组、格列本脲组、吡那地尔组、冠心康组、冠心康加格列本脲组。采用酶解法分离大鼠心室肌细胞,用无钙台式液灌流10 min、停灌30 min、再灌注45 min模拟心肌缺血再灌注损伤。将药物直接加入细胞液中（格列本脲10μmol/L、吡那地尔50μmol/L、冠心康注射液1 ml/L）充分作用后,4℃放置24 h。采用实时荧光定量多聚酶链式反应法及蛋白质印迹法检测各组心肌细胞K_（ATP）亚基Kir6.1、Kir6.2、SUR2A和SUR2B的mRNA表达及蛋白含量。结果：正常大鼠心肌细胞可见SUR2A、Kir6.1和Kir6.2蛋白及mRNA的表达,而SUR2B蛋白几乎不表达。模型组K_（ATP）各个亚基蛋白及mRNA的表达均较正常组有一定程度的增加。与模型组比较,吡那地尔可显著增加K_（ATP）各亚基mRNA及蛋白的表达,格列本脲可阻断这一作用;冠心康可明显增加K_（ATP）通道各亚基mRNA及蛋白的表达。结论：复方冠心康具有明显的促进K_（ATP）开放的作用,从而起到心血管保护作用。     

牛膝-杜仲成分组合干预糖皮质激素性骨质疏松模型小鼠的研究

目的 探讨牛膝成分β-蜕皮甾酮（βEcdysterone，βEcd）联合杜仲成分松脂醇二葡萄糖苷（pinoresinol diglucoside，PDG）治疗糖皮质激素性骨质疏松症的可行性。方法 2月龄SPF级雄性C57BL/6小鼠分为正常对照组、模型组、阿仑膦酸钠（ALN）组、βEcd组、PDG组和βEcd+PDG组。对照组皮下注射100μL生理盐水；模型组与给药组皮下注射地塞米松（2 mg/kg）；给药组中，分别皮下注射ALN（0.5 mg/kg）、βEcd（0.5 mg/kg）、PDG（0.5 mg/kg）以及βEcd+PDG（剂量各为0.5 mg/kg）。每周测量体重，计算体质量指数；4周实验结束后以Micro CT、生物力学、ELISA、Western blot方法评估模型及治疗效果。结果 与对照组比较，模型组体质量指数、皮质骨骨矿物质密度（BMD）、股骨弹性模量、弯曲刚度、弯曲强度及最大负重载荷、骨形成标志物P1NP浓度降低（P＜0.05），骨吸收标志物β-CTx浓度升高（P＜0.05），骨组织细胞凋亡相关蛋白Caspase-3、Bax表达增高（P＜0.05）；与模型组比较，βEcd-PDG组合提高模型小鼠体质量指数、BMD、股骨弯曲强度和最大负重载荷、P1NP浓度（P＜0.05），降低β-CTx浓度（P＜0.05），上调抗凋亡因子Bcl-2表达、下调Caspase-3、Bax表达（P＜0.05）。结论 βEcd-PDG组合促进GIOP模型小鼠骨形成，增加骨密度、增强骨质量，并可改善骨组织细胞的凋亡水平。     

Astragaloside IV Regulates Expression of ATP-sensitive Potassium Channel Subunits after Ischemia-reperfusion in Rat Ventricular Cardiomyocytes

Objective: Astragaloside IV (AsIV) is the major effective component extracted from the Chinese herb Astragalus membranaceus, which has been widely used to treat cardiovascular disease. Recent studies have shown that AsIV can potentially protect the heart from myocardial ischemic injury, but the mechanisms of action are unknown. ATP-sensitive potassium (KATP) channels are activated during ischemia and exert a compensatory protective effect on cardiomyocytes. We therefore examined the effects of AsIV on KATP channel currents and channel expression in isolated rat ventricular cardiomyocytes after ischemia-reperfusion injury. Methods: Forty Wistar rats were divided into five groups: control group, ischemia-reperfusion (IP) group, IP + glibenclamide group, IP + pinacidil group and IP + AsIV group. The ischemia-reperfusion injury model was established in enzymatically isolated ventricular cardiomyocytes by perfusion with calcium-free Tyrode solution for 10 min, arrest for 30 min, and reperfusion for 45 min. The different drugs were applied for 10-15 min, and the KATP channel current (IKATP) was recorded with voltage-clamp mode by whole-cell patch-clamp technique. Protein and mRNA expression of the KATP channel subunits Kir6.1, Kir6.2, SUR2A and SUR2B was quantified using western blotting and real-time PCR. Results: The KATP current in IP group was significantly greater than that in control group (211.45±33.67 vs 83.51±23.67 pA; P<0.01). Glibenclamide (10 μmol/L) blocked KATP currents, whereas both AsIV (1 mg/L) and the known channel opener pinacidil (50 μmol/L) significantly increased IKATP (P<0.05). Consistent with this, AsIV significantly up-regulated protein and mRNA expression of Kir6.1, Kir6.2, SUR2A, SUR2B (P<0.01 vs IP group). Conclusion: The protective effects of AsIV in ischemia-reperfusion injury may be related to the up-regulation of several KATP channel subunits and facilitation of KATP currents.