Nantong Medical College

Yancheng, China

Nantong Medical College

Yancheng, China
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Ge X.-H.,Soochow University of China | Ge X.-H.,First Peoples Hospital of Xuzhou | Zhu G.-J.,Soochow University of China | Geng D.-Q.,Xuzhou Medical College | And 2 more authors.
Neurological Sciences | Year: 2012

The aim of this study was to determine the mechanism by which erythropoietin (EPO) suppressed 6-hydroxydopamine (6-OHDA)-induced apoptosis. Our results showed that 6-OHDA remarkably decreased phosphorylation of glycogen synthase kinase 3β (GSK3β) as well as enhanced the level of Bax in the mitochondria. Besides, 6-OHDA decreased the mitochondrial expression of Bcl-2 without altering the cytoplasmic expression of Bcl-2. In line with these results, 6-OHDA treatment enhanced the apoptosis and caspase 3 activity in PC12 cells. These findings indicated that mitochondrial dysfunction was involved in the neurotoxicity of 6-OHDA and GSK3β might act upstream of Bax/Bcl-2 and the caspase 3 pathways in 6-OHDA-treated PC12 cells. Furthermore, EPO reduced 6-OHDA-induced growth inhibition. Western blot exhibited that GSK3β inhibitor 4-benzyl-2-methyl-1, 2,4-thiadiazolidine-3, 5-dione (TDZD8) and EPO not only increased the phosphorylation of GSK3β but also inhibited the mitochondrial translocation of Bax. In agreement with these results, EPO and TDZD8 obviously increased the mitochondrial expression of Bcl-2. Finally, TDZD-8 and EPO significantly suppressed the enhanced apoptosis and activity of caspase 3 induced by 6-OHDA. Taken together, GSK3β-mediated mitochondrial cell death pathway is involved in the neuroprotective effect of EPO against 6-OHDA-induced apoptosis. © The Author(s) 2011.


Tao J.,Nanjing Medical University | Wu D.,Nanjing Medical University | Wu D.,Nantong Medical College | Li P.,Nanjing Medical University | And 3 more authors.
Molecular Medicine Reports | Year: 2012

The miR-17-92 cluster has long been recognized as an oncogenic microRNA (miRNA) cluster and is amplified in multiple cancers. However, the individual roles of its members in carcinogenesis are largely undetermined. After transfection of miR-18a mimics, an antisense oligonucleotides inhibitor, siRNAs and a luciferase reporter plasmid, the MTT assay, colony formation assay, semi-quantitative RT-PCR, luciferase assay and Western blot analysis were conducted in bladder cancer cells. In the present study, we showed that miR-18a, a member of the miR-17-92 cluster, suppressed cell proliferation in bladder cancer T24 cells. Furthermore, ectopic expression of miR-18a in T24 cells down-regulated Dicer expression at both the mRNA and protein level, while inhibition miR-18a by antisense oligonucleotides could enhance Dicer expression in T24 cells. Two binding sites of miR-18a were found in Dicer 3' untranslated region (3' UTR). Luciferase reporter assay demonstrated that both sites could mediate expression suppression in vitro. In addition, knockdown of Dicer expression by siRNA mimicked cell growth suppression induced by miR-18a in T24 cells. These results show that miR-18a functions as a tumor suppressor by targeting Dicer in bladder cancer T24 cells and revealed a noteworthy feedback loop, which may be utilized by the miR-17-92 cluster to control miRNA output and prevent its overexpression.


PubMed | Nantong Medical College
Type: Journal Article | Journal: Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology | Year: 2010

To investigate the effect of Safflor yellow on the gene expression of neuronal nitric oxide synthase (nNOS), inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) in neonatal asphyxia.30 minutes after SY 7 g/kg weight intraperitoneally was administered on the neonatal rats. After asphyxia for 40 minutes,the neonatal rats were reoxygenated for 48 h, and the nitric oxide synthases (NOSs) mRNA expression was assessed by semi-quantitative reverse transcription-polymerase chain reaction.Neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS) were up in hypoxia/reoxygenation (H/R) 48 h group, while both of them were down significantly in SY group, but no change was observed on endothelial nitric oxide synthase (eNOS).The protective of SY from brain damage induced by neonatal asphyxia might be associated with expression of NOSs mRNA.

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