Albumin resuscitation protects against traumatic/hemorrhagic shock-induced lung apoptosis in rats

Objective: To determine the effects of albumin administration on lung injury and apoptosis in traumatic/hemorrhagic shock (T/HS) rats. Methods: Studies were performed on an in vivo model of spontaneously breathing rats with induced T/HS; the rats were subjected to femur fracture, ischemia for 30 min, and reperfusion for 20 min with Ringer’s lactate solution (RS) or 5% (w/v) albumin (ALB), and the left lower lobes of the lungs were resected. Results: Albumin administered during reperfusion markedly attenuate...     

Berbamine inhibits proliferation and induces apoptosis of KU812 cells by increasing Smad3 activity

Objective  

The cytotoxic effect of berbamine on chronic myeloid leukemia (CML) cell line KU812 was evaluated, and the mechanisms of its action were explored.     

Review:Mechanism of acute pancreatitis complicated with injury of intestinal mucosa barrier

Acute pancreatitis (AP) is a common acute abdomen in clinic with a rapid onset and dangerous pathogenetic condition. AP can cause an injury of intestinal mucosa barrier, leading to translocation of bacteria or endotoxin through multiple routes, bacterial translocation (BT), gutorigin endotoxaemia, and secondary infection of pancreatic tissue, and then cause systemic in- flammatory response syndrome (SIRS) or multiple organ dysfunction syndrome (MODS), which are important factors influencing AP’s severity and mortality. Meanwhile, the injury of intestinal mucosa barrier plays a key role in AP’s process. Therefore, it is clinically important to study the relationship between the injury of intestinal mucosa barrier and AP. In addition, many factors such as microcirculation disturbance, ischemical reperfusion injury, excessive release of inflammatory mediators and apoptosis may also play important roles in the damage of intestinal mucosa barrier. In this review, we summarize studies on mechanisms of AP.     

Proapoptotic and pronecrosis effect of different truncated hepatitis C virus core proteins

Objective: To study the roles of different truncated hepatitis C virus (HCV) core proteins (CORE) in the pathogenesis of HCV persistent infection and hepatocellular carcinoma (HCC) and to assess intracellular localization in transiently transfected cells. Methods: Seven truncated CORE-GFP (green fluorescent protein) fusion protein expression plasmids were constructed,which contained HCV CORE sequences derived from tumor tissues (BT) and non-tumor tissues (BNT) from one patient infected with HCV. Amino acid (aa) lengths were BT: 1-172 aa, 1-126 aa, 1-58 aa, 59-126 aa, 127-172 aa; BNT: 1-172 aa and C191:1-172 aa respectively. Subcellular localization of CORE-GFP was analyzed by con-focal laser scanning microscope. Apoptosis and necrosis were quantified by flow cytometry. Results: Different truncated CORE-GFP localized mainly in the cytoplasm, but nuclear staining was also observed. HCV CORE could induce apoptosis and necrosis, and different truncated COREs could induce cell apoptosis and necrosis at different levels. Among the same length 1-172 aa of BT, BNT and C191, the cell apoptosis and necrosis percentage of BT is highest, and C191 is the lowest (BT＞BNT＞C191). To the different fragment COREs of BT,N-terminal of CORE induced apoptosis and necrosis higher, compared with that of C-terminal (1-172 aa＞1-126 aa＞1-58aa＞ 127-172 aa＞59-126 aa). Conclusion: These results suggest HCV CORE could induce apoptosis and necrosis of cells, which might play an important role in the pathogenesis of HCV persistent infection and HCC and the different CORE domains of different HCV quasi-species might have some difference in their pathogenesis.     

In vitro study of immunosuppressive effect of apoptotic cells

INTRODUCTION Apoptosis plays an important role in differen- tiation, development and pathophysiological proc- esses such as inflammation, neoplasia and autoim- mune diseases. For a long time, apoptotic cells per se and the clearance of apoptotic cells had been viewed as neutral in immune response. Recently many in- vestigations suggested that apoptotic cells actively regulate the immune response (Voll et al., 1997; Fadok et al., 1998; 2000; Byrne and Reen, 2002). Apoptotic cells release …     

Chlorella vulgaris triggers apoptosis in hepatocarcinogenesis-induced rats

Chlorella vulgaris (CV) has been reported to have antioxidant and anticancer properties. We evaluated the effect of CV on apoptotic regulator protein expression in liver cancer-induced rats. Male Wistar rats (200∼250 g) were divided into eight groups: control group (normal diet), CDE group (choline deficient diet supplemented with ethionine in drinking water to induce hepatocarcinogenesis), CV groups with three different doses of CV (50, 150, and 300 mg/kg body weight), and CDE groups treated with different doses of CV (50, 150, and 300 mg/kg body weight). Rats were sacrificed at various weeks and liver tissues were embedded in paraffin blocks for immunohistochemistry studies. CV, at increasing doses, decreased the expression of anti-apoptotic protein, Bcl-2, but increased the expression of pro-apoptotic protein, caspase 8, in CDE rats, which was correlated with decreased hepatoctyes proliferation and increased apoptosis as determined by bromodeoxy-uridine (BrdU) labeling and terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling (TUNEL) assay, respectively. Our study shows that CV has definite chemopreventive effect by inducing apoptosis via decreasing the expression of Bcl-2 and increasing the expression of caspase 8 in hepatocarcinogenesis-induced rats. Project supported by Department of Biochemistry, Faculty of Medicine, UKM Medical Center, Universiti Kebangsaan Malaysia, and the Malaysian Ministry of Science and Technological Innovation (MOSTI)     

停训28周大鼠海马VEGF表达的免疫组织化学研究

本文以不同强度训练大鼠停训28周为对象,应用免疫组织化学技术探讨长期停训对大鼠脑组织的影响。采用雄性SD大鼠(3月龄,由西安交通大学医学院动物管理中心提供)24只,体重248±24g,国家标准啮齿类动物干燥饲料喂养,自由饮食,温度22℃~27℃,湿度40%~60%。适应性喂养1周后进行实验。将大鼠随机分为安静对照组、有氧训练组和疲劳训练组,每组各8只。有氧训练组和疲劳训练组运动负荷参照B ed ford跑台训练模型训练8周。8周后疲劳训练组和有氧训练组停训,与对照组同处于正常笼内生活状态,再饲养28周。各组大鼠依次用乌拉坦腹腔麻醉,开胸行左心室穿刺灌注,同时剪破右心耳放血.灌注过程中,先用加3‰肝素生理盐水灌注15m in左右,直至流出液体为粉红色时换用中性甲醛固定液灌注40m in左右,pH=7.4,将灌注好的标本置于事先准备的冰盘上并迅速取材。得出结论为大鼠恢复28周后有氧、疲劳训练使海马CA1区的表达增强,未见显著性差异。显示该区在训练恢复后VEGF阳性表达基本恢复。海马CA3区,VEGF的表达下降趋势显著。     

刺五加注射液对 Hela 细胞抑制作用的实验研究

目的:探讨刺五加注射液对人宫颈癌细胞株Hela体外增殖的抑制作用。方法:采用MTT法测定了不同浓度的刺五加注射液对人宫颈癌细胞株Hela的体外抑制作用,倒置显微镜观察细胞形态变化。结果:刺五加注射液浓度越高对Hela细胞抑制作用越好,作用时间越长抑制效果越强,量效关系和时效关系良好;形态学观察到细胞凋亡。结论:刺五加注射液对人宫颈癌细胞株Hela的细胞增殖有较强的抑制作用。     

新城疫病毒体外诱导S180细胞凋亡的实验研究

目的:探讨新城疫病毒(Newcastle disease virus,NDV)体外对S180肉瘤细胞(简称S180)生长有无抑制和诱导细胞凋亡作用。方法:取培养至对数生长期的S180细胞浓度为5×104/mL和1×106/mL分别接种于96孔板和50mL培养瓶中,加入不同浓度的NDV(1∶20、1∶10、1∶5)作用24h,分别用MTT法检测NDV对S180瘤细胞的生长抑制作用,荧光显微镜和琼脂糖凝胶电泳检测细胞凋亡。结果:经上述不同浓度的NDV作用24h,对S180细胞生长的抑制率依次为10%、26%、39%,各实验组吸光度值(A490)与对照组比较差异均有统计学意义(P<0.05)。荧光显微镜观察实验组培养的S180瘤细胞,出现细胞核固缩及凋亡小体,琼脂糖凝胶电泳见DNA梯形条带。结论:NDV对体外培养S180细胞增殖有明显抑制作用,可诱导S180细胞凋亡。