ABSTRACT
<p><b>OBJECTIVE</b>To observe the impact of specific short hairpin RNA (shRNA) targeting survivin gene on tumorigenesis and angiogenesis of human brain glioblastoma U251 cells in vivo of nude mice.</p><p><b>METHODS</b>U251 cells, U251-SR cells transfected stably with shRNA eukaryotic expression vector pWH1-SR targeting survivin gene, and U251-P cells transfected stably with blank pWH1 vector, were inoculated respectively into subcutaneous tissue in flank of 15 nude mice (each group 5 mice), and the tumor growth status was observed and measured. Protein expressions of survivin, proliferating cell nuclear antigen (PCNA) and factor VIII related antigen (F VIII RAg) were investigated by immunohistochemistry SABC method, apoptotic cells were screened by TUNEL method, furthermore proliferative index (PI), apoptotic index (AI) and microvessel density (MVD) were measured respectively in each group of tumor specimens.</p><p><b>RESULTS</b>Comparing with those in U251 and U251-P groups, in U251-SR group, the tumorigenesis time delayed, tumor grew slowly, both tumor volume and tumor weight decreased significantly (P < 0.01 for both); Survivin protein expression was down-regulated markedly; PI and MVD decreased significantly, whereas AI increased remarkably (P < 0.01 for all).</p><p><b>CONCLUSIONS</b>The specific shRNA targeting survivin gene can inhibit significantly tumorigenesis and angiogenesis of U251 cells in vivo.</p>
Subject(s)
Animals , Female , Humans , Male , Mice , Apoptosis , Brain Neoplasms , Metabolism , Pathology , Cell Line, Tumor , Glioblastoma , Metabolism , Pathology , Inhibitor of Apoptosis Proteins , Mice, Nude , Microtubule-Associated Proteins , Genetics , Neoplasm Transplantation , Neovascularization, Pathologic , Pathology , RNA Interference , RNA, Small Interfering , Genetics , Repressor Proteins , TransfectionABSTRACT
Objective:To determine whether heme oxygenase-2(HO-2) gene deletion can attenuate oxidative injury induced by free Fe2+. Methods:Stereotactic injection of 10 μl sterile FeCl2 (10 mmol/L) was made into the right striata of HO-2 knockout mice and wild-type mice. Brain edema severity was measured at 24 h. Cell viability, protein oxidation, and lipid oxidation of the basal ganglia were determined at 72 h. Western blot analysis was applied for heme oxygenase-1 (HO-1) measurement.Results: Brain water content significantly decreased in HO-2 knockout mice at 24 h compared with wild-type mice. Protein oxidation and lipid oxidation significantly decreased in HO-2 knockout mice at 72 h compared with wild-type mice, while the striatal cell viability increased significantly. HO-1 expression at baseline and 72 h was also similar to that in wild-type mice. Conclusion:These results show that HO-2 gene deletion can protect basal ganalia cells from free Fe2+ -mediated oxidative stress injury,suggesting that selective inhibition of HO-2 may have a protective effect on brain oxidative injury.
ABSTRACT
Objective:To determine whether heme oxygenase-2(HO-2) gene deletion can attenuate oxidative injury induced by free Fe2+. Methods:Stereotactic injection of 10 μl sterile FeCl2 (10 mmol/L) was made into the right striata of HO-2 knockout mice and wild-type mice. Brain edema severity was measured at 24 h. Cell viability, protein oxidation, and lipid oxidation of the basal ganglia were determined at 72 h. Western blot analysis was applied for heme oxygenase-1 (HO-1) measurement.Results: Brain water content significantly decreased in HO-2 knockout mice at 24 h compared with wild-type mice. Protein oxidation and lipid oxidation significantly decreased in HO-2 knockout mice at 72 h compared with wild-type mice, while the striatal cell viability increased significantly. HO-1 expression at baseline and 72 h was also similar to that in wild-type mice. Conclusion:These results show that HO-2 gene deletion can protect basal ganalia cells from free Fe2+ -mediated oxidative stress injury,suggesting that selective inhibition of HO-2 may have a protective effect on brain oxidative injury.
ABSTRACT
<p><b>OBJECTIVE</b>To evaluate protective effects of Rheum tanguticum polysaccharides (RTP) on traumatic brain injury (TBI) in rats.</p><p><b>METHOD</b>The polysaccharides (RTP) were extracted from Tanguficum Maxim. 120 rats were divided into 15 groups, with 8 rats in each group. RTP at 100, 200 and 400 mg x kg(-1) were administrated orally once a day for five days, and model of brain injury was made by dropping weight method.</p><p><b>RESULT</b>RTP reduced water content and malondialdehyde (MDA) levels, and increased total SOD activity and Na+-K+ ATPase activity after injuried.</p><p><b>CONCLUSION</b>The polysaccharides may be one of the effective comptents in Rheum tanguticum, showing significant neuroprotective effects.</p>