L-type calcium current (ICa-L) alterations are implicated in various cardiac diseases, and the lysophosphatidic acid (LPA) level increases in several ischemic heart diseases. We investigated the effects of LPA on ICa-L in normal and H2O2-treated neonatal rat ventricular myocytes. LPA treatment (24 h) increased the action potential duration (APD) and ICa-L in normal ventricular myocytes, but it decreased these parameters in H2O2-treated myocytes. LPA increased the single-channel open probability of L-type calcium channels in both normal and H2O2-treated myocytes. LPA activated calcineurin (CaN) and induced the cytoplasm-to-nucleus translocation of nuclear factor of activated T-cells (NFAT) in H2O2-treated cardiomyocytes. In H2O2-treated cardiomyocytes, LPA decreased Ca(v)1.2 mRNA and protein expression levels at 4 and 8 h, respectively. A CaN inhibitor (FK-506) prevented LPA-induced APD, ICa-L, and Ca(v)1.2 mRNA and protein down-regulation. The LPA-induced ICa-L increase in normal cardiomyocytes was CaN-NFAT signaling-independent, and LPA did not affect Ca(v)1.2 mRNA or protein expression. In conclusion, LPA increases the ICa-L, in normal ventricular myocytes by increasing the single-channel open probability of L-type calcium channels, and LPA decreases ICa-L in H2O2-treated cardiomyocytes via the CaN-NFAT pathway. (C) 2015 Published by Elsevier Inc.

Objective To investigate the role of recombinant human Elafin in the pathogenesis of hepatic ischemia-reperfusion injury(HIRI).Methods All rats were divided into 5 groups randomly,sham-operation group,model group,Elafin treatment groups(high,middle and low doses),10 cases in each group.Elafin was given with high,middle and low doses in Elafin treatment groups.The rat model of HIRI was made.The contents of serum ALT,AST and LDH and liver MPO and NO were determined after the injection of Elafin.Meanwhile,the hepatic histopathological changes were observed.Results The liver showed severe hepatocytic damage after HIRI and the contents of serum ALT,AST and LDH and liver MPO and NO were significantly risen(P < 0.001).The injection of Elafin before operation could make the level of ALT,AST,LDH,MPO and NO significantly dropped(P < 0.05).Conclusion The recombinant human Elafin has a protective effect on the rat HIRI to some extent.

目的 探讨三萜类化合物熊果酸(UA)对人膀胱癌T-24细胞增殖、迁移及裸鼠皮下移植瘤生长的抑制作用及其机制.方法 应用熊果酸处理体外培养的人膀胱癌T-24细胞,四甲基偶氮唑蓝(MTT)比色法、细胞迁移法检测UA对T-24细胞的增殖抑制效应;建立膀胱癌皮下移植瘤模型,观察UA对移植瘤的生长抑制作用.结果 体内﹑外实验结果显示:各治疗组UA能较明显抑制T-24细胞增殖、迁移,并在48 h抑制作用明显.在体内使裸鼠皮下移植瘤体积明显缩小,并表现具有一定的剂量-时间依赖关系.结论 UA能明显抑制肿瘤细胞生成,其作用靶点可能为肿瘤新生血管内皮细胞.

Objective To investigate the role of neutrophil elastase inhibitor(Elafin) in pathogenesis of hepatic ischemia-reperfusion injury(HIRI).Methods The rat model of hepatic ischemia-reperfusion was administrated with Elafin at different doses,and then the levels of ALT,AST and LDH in serum were measured.Meanwhile,pathohistological changes in liver were examined.Results The rats showed severe hepatocytic damage after hepatic ischemia-reperfusion and serum levels of ALT,AST and LDH were significantly raised(P 0.001).However,those symptoms could be relieved to some extent by preoperative injection of Elafin.Conclusion Neutrophil elastase inhibitor Elafin has a protective effect against hepatic ischemia-reperfusion injury in rats.

目的 探讨重组蛋白酶抑制剂(recombinant proteinase inhibitor,RPI)对大鼠胰腺缺血再灌注(I/R)损伤的保护作用.方法 Wistar大鼠30只随机分为假手术组、I/R模型组和RPI组,分别测定各组大鼠血清淀粉酶、脂肪酶含量.检测各组血清中肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β) 的变化.结果 RPI组的淀粉酶、脂肪酶含量较模型组显著降低(P<0.01);RPI组可明显降低模型组大鼠血清TNF-α、IL-1β(P<0.01) 的水平.结论 RPI可以抑制大鼠胰腺I/R损伤所致的急性炎性反应,对大鼠胰腺I/R损伤有保护作用.

Objective To determine the therapeutic effect of rhKD/APP var on acute necrosis pancreatitis in rats.Methods Acute necrosis pancreatitis was induced by injections of odium taurocholate into the main pancreaticduct of rats.Serum amylase and lipase activities of the rats were assayed and histopathological changes were observed after treatment with rhKD/APP var.Results rhKD/APP var inhibited the serum amylase and lipase activities remarkably and ameliorated the histopathological changes of the pancreas.Conclusion rhKD/APP var can suppress pathogenesis of the acute necrosis pancreatitis in rats.