生脉四物汤对肥厚型心肌病IGF-1的影响

目的观察生脉四物汤对肥厚型心肌病(HCM)病人胰岛素样生长因子-l(IGF1)的影响.方法正常对照组20例,中药治疗组20例.治疗组口服生脉四物汤,每日1剂,连续服20 d.用放射免疫法测定血清IGF-1水平,观察用药前对照组与治疗组血清IGF-1水平,比较治疗组用药10 d、20 d后与用药前血清IGF-1水平的变化.结果用药前治疗组血清IGF-1水平显著高于对照组(P＜0.001);治疗组用药10 d后血清IGF-1水平有下降趋势(P＜0.05),用药20 d后血清IGF-1水平明显低于用药前(P＜0.01).结论生脉四物汤能明显降低HCM病人血清IGF-1水平,提示生脉四物汤对HCM有较好的治疗作用.     

血清胱蛋白酶抑制剂C诊断老年高血压早期肾损害

目的 观察老年高血压患者血清胱蛋白酶抑制剂C(Cyst-c)浓度对检出早期肾损害的价值。方法 对412例老年高血压患者同时测血Cyst-c和血肌酐(Cr)浓度，并与正常对照组对照。结果412例老年高血压患者中早期肾损害197例(占47.82％)，肾功能不全24例(5.82％)，肾功能正常191例(46.36％)。在早期肾损害组：血Cyst-c浓度明显高于对照组[(2.3±0.8 vs 0.9±0.2)mg／L，P＜0.01)]，而血Cr浓度两组无显著性差异[(86.6±12.7 vs 81.0±10.5)μmol／L，P＞0.05]。结论 老年高血压患者中，早期肾损害占47.82％，很常见。血Cyst-c能检出血Cr不能检出的早期肾损害。     

硝酸甘油耐受对心肌缺血/再灌注损伤影响的研究

目的验证硝酸甘油(GTN)耐受对耐受产生后的心肌缺血/再灌注损伤的影响。方法雄性SD大鼠随机分组,分别接受GTN[600μg/(kg.h)]或生理盐水静脉滴注12h。检验耐受的产生,耐受和对照大鼠接受40min缺血和4h再灌注。检测心肌细胞凋亡(TUNEL法)、心肌坏死面积(Evansblue-TTC染色)和血清肌酸激酶(CK)、乳酸脱氢酶(LDH)活性。结果与单纯心肌缺血/再灌注相比,硝酸甘油耐受引起了再灌注后心肌凋亡比例、心肌坏死面积和血清心肌酶活性的显著增高,而单纯耐受没有对心脏造成明显损伤。结论实验结果提示除了使心血管对硝酸甘油的敏感性降低外,耐受对再灌注心脏存在一种潜在的损伤作用。     

干扰素α干预对大鼠胰腺纤维化的影响

目的 观察干扰素α(INF-α)对DDC诱导的胰腺纤维化大鼠模型纤维增生程度、胰腺星状细胞活化标志物α-平滑肌肌动蛋白(α-SMA)和细胞外基质成分Ⅲ型胶原蛋白表达的影响.方法 Wistar大鼠40只随机数字法分成对照组、纤维化组和干扰素组.纤维化组和干扰素组每周2次腹腔内注射DDC,干扰素组在造模同时每天皮下注射INF-α10万U.6周末取材,光镜下观察胰腺病理学变化.免疫组化法测定胰腺组织中α-SMA、Ⅲ型胶原蛋白的表达.结果 第4周起纤维化组大鼠体重增长缓慢甚至下降,干扰素组体重仍缓慢增长,5周后两组差异显著[(309.8±19.7)g与(277.3±19.9)g,P＜0.05].纤维化组胰腺组织纤维化表现明显,纤维化分值、Masson染色值、α-SMA和Ⅲ型胶原蛋白相对表达量分别为2.679±0.899、218.713±36.102、148.971±30.686和88.142±42.581;干扰素组纤维化减轻,上述指标分别为1.952±0.219、114.732±24.912、77.237±9.275和59.952±25.498,均较纤维化组显著降低(P＜0.05).结论 给予INF-α能显著减轻纤维化程度和α-SMA、Ⅲ型胶原表达,对DDC诱导的大鼠胰腺纤维化有一定的预防作用.     

糖耐量减低与心血管疾病及阿卡波糖作用

Impaired glucose tolerance(IGT) is a clinical state between normal and abnormal glucose metabolism with increased risk of cardiovascular disease. Its mechanism mainly related to insulin resistance, oxidative stress ,blood hypercoagulability, inflammatory response ,as well as related lipotoxieity. α-glucosidase inhibitor acarbose is safe and effective to reduce postprandial hyperglycemia, and has been approved for the treatment of patients with IGT. A growing number of studies have shown that acarbose also has cardiovascular benefit.     

小儿脑性瘫痪脑血流动力学的研究

目的研究小儿脑性瘫痪(脑瘫)脑血流动力学的变化规律.方法应用经颅多普勒超声对347例脑瘫患儿与30例正常健康儿脑血流动力学参数进行对照检测.结果脑瘫患儿的大脑前动脉、大脑中动脉、大脑后动脉的平均血流较同年龄段的正常小儿显著下降(P＜0.05),而脑血管阻力指数则显著增高(P＜0.05).小于1岁年龄组的平均流速下降及脑血管阻力指数增高较其他年龄组更显著(P＜0.05).结论脑瘫患儿存在脑血流动力学的高阻力、低灌注障碍,早期应用改善脑微循环治疗对于小儿脑瘫的治疗有重要意义.     

An oncolytic adenoviral vector of Smac increases antitumor activity of TRAIL against HCC in human cells and in mice

Hepatocellular carcinoma (HCC) displays a high resistance to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated cell death. To increase sensitivity of HCC cells to TRAIL, we have constructed an oncolytic adenoviral vector (ZD55) and used this vector to deliver second mitochondria-derived activator of caspases (Smac) and TRAIL genes (ZD55-Smac and ZD55-TRAIL, respectively) into HCC cells. Our data showed that human HCC cells express high levels of inhibitor of apoptosis proteins (IAPs). Transfected HCC cells expressing exogenous X-linked IAPs (XIAPs) displayed more resistance to TRAIL. The expression of Smac led to rapid and potent activation of apoptosis in HCC cells after infection with ZD55-Smac. The activation of caspases and induction of apoptosis could be enhanced further through coinfection with ZD55-TRAIL. The combined treatment of ZD55-Smac and ZD55-TRAIL resulted in significant reduction of XIAP expression levels. In addition, our in vivo data in mice showed only a partial response in the established tumor treated either by ZD55-Smac or ZD55-TRAIL alone. By contrast, complete tumor regression was observed by combination of ZD55-Smac and ZD55-TRAIL in all treated animals. This strong antitumoral activity achieved by this combination was due to a dramatic induction of tumor cell apoptosis in the treated tumors. In conclusion, our data indicate that Smac antagonizes the IAPs in HCC tumor cells and enhances tumor cell death induced by TRAIL in the oncolytic adenoviral vector. The combination of Smac and TRAIL delivered by way of the oncolytic adenoviral vector would provide a useful strategy for therapy of HCC and might also be applied to other IAPs abundant in cancers.     

Down-modulation of heat shock protein 70 and up-modulation of Caspase-3 during schisandrin B-induced apoptosis in human hepatoma SMMC-7721 cells

AIM: To investigate the effect of schisandrin B (Sch B) on proliferation and apoptosis of human hepatoma SMMC-7721 cells in vitro and regulation of Hsp70 and Caspases-3, 7, 9 expression by Sch B. METHODS: Human hepatoma cell line SMMC-7721 was cultured and treated with Sch B at various concentrations. Growth suppression was detected with MTT colorimetric assay. Cell apoptosis was confirmed by DNA ladder detection and flow cytometric analysis. The expression of Hsp70, Caspases-3, 7, 9 were analyzed by Western blot analysis. RESULTS: Sch B inhibited the growth of hepatoma SMMC-7721 cells in a dose-dependent manner, leading to a 50% decrease in cell number (LC50) value of 23.50 mg/L. Treatment with Sch B resulted in degradation of chromosomal DNA into small internucleosomal fragments, evidenced by the formation of a 180-200 bp DNA ladder on agarose gels. FCM analysis showed the peak areas of subdiploid at the increased concentration of Sch B. The results of Western bolt analysis showed that Hsp70 was down-regulated and Caspase-3 was up-regulated, while the activity of Caspases-7, -9 had no significant change. CONCLUSION: Sch B is able to inhibit the proliferation of human hepatoma SMMC-7721 cells and induce apoptosis, which goes through Caspase-3-dependent and Caspase-9-independent pathway accompanied with the down-regulation of Hsp70 protein expression at an early event.