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Xinxiang, China

Ren Z.-P.,Huazhong University of Science and Technology | Ren Z.-P.,Xinxiang Center Hospital | Sun L.-P.,Huazhong University of Science and Technology | Xia Y.-C.,Huazhong University of Science and Technology | Tong Q.-X.,Huazhong University of Science and Technology
Journal of Huazhong University of Science and Technology - Medical Science | Year: 2013

The activation of hepatic stellate cells (HSCs) and their transformation to myofibroblasts are the key steps in the pathological progress of liver fibrosis. The transforming growth factor-β (TGFβ)/Smad pathway is involved in the proliferation and collagen synthesis of HSCs. This study aimed to examine the effect of the protease inhibitor MG132 on the signaling pathway of TGFβ/Smad in HSC-T6 cells and seek a novel therapeutic approach for liver fibrosis. The HSC-T6 cells were treated with MG132 at different concentrations (0-10 μmol/L). Cell proliferation was detected by MTT method. The mRNA and protein expression levels of TGFβ1, Smad3 and Smad7 were determined in HSC-T6 cells by real-time PCR and Western blotting, respectively, after treatment with MG132 at different concentrations (1, 2, 3 μmol/L) or RPMI1640 alone (serving as control). The results showed that MG132 could inhibit the proliferation of HSC-T6 cells in a dose-dependent manner, and the IC 50 of MG132 was 6.84 μmol/L. After treatment with MG132 at 1, 2 or 3 μmol/L for 24 h, the mRNA expression levels of TGF-β1 and Smad3 were significantly decreased (P<0.05), but the Smad7 mRNA expression had no significant change (P>0.05). There was also a significant decrease in the protein expression level of TGF-β1 and Smad3 (P<0.05). However, the expression of Smad7 protein was substantially increased when compared with the control group (P<0.05). It was concluded that the inhibition of TGFβ/Smad pathway in HSC-T6 cells by MG132 can reduce the production of profibrosis factors (TGFβ1, Smad3) and promote the expression of anti-fibrosis factor (Smad7), suggesting that MG132 may become a potential therapeutic alternative for liver fibrosis. © 2013 Huazhong University of Science and Technology and Springer-Verlag Berlin Heidelberg.

Yue W.,Xinxiang Center Hospital
Interventional Neuroradiology | Year: 2011

We report the clinical and angiographic results of endovascular treatment of unruptured intracranial aneurysms. Over a three-year period, 80 unruptured aneurysms in 74 patients were electively treated with endovascular management. One aneurysm was diagnosed during investigations for a second ruptured aneurysm, 54 aneurysms were incidentally discovered, 18 aneurysms presented with symptoms of mass effect and seven aneurysms presented with symptoms of brain stem ischemia. Mean size of the 80 unruptured aneurysms was 12.5±8.0 mm (range, 2-39 mm). Thirty-six aneurysms (45%) were small (<10 mm), 38 aneurysms (47.5%) were large (10-25 mm), and six aneurysms (7.5%) were giant (25-39 mm). Forty-eight wide-necked aneurysms (60%) were coiled with the aid of a supporting device. The mortality rate was 1.25%, and the overall morbidity was 1.25%. Of these, one of the patients suffered a stroke, leading to severe disability (1.25%). In one patient, the aneurysm ruptured during treatment, resulting in death. Initial aneurysm occlusion was complete (100%) in 76.25% aneurysms, nearly complete (90%-98%) in 10% aneurysms and incomplete (60%-85%) in 13.75% aneurysms. Follow-up angiography was available in 67 patients with 73 treated aneurysms (91.25%) from one to 36 months (mean 9.3 months); partial reopening occurred in 7.5%, mainly large and giant aneurysms (5.5%). Additional coiling was performed in four aneurysms. There were no complications in additional treatments. At 14.1-month clinical follow-up (range, 2 to 36 months), mRS score was 0 in 78.75% patients, 1 in 10% patients, 2 in 8.75% and 3 in 1.25%. There was no aneurysmal rup-ture during the follow-up period. Endovascular treatment of unruptured intracranial aneurysms has low procedural mortality and morbidity rates.

Feng X.-S.,Henan University of Science and Technology | Wang Y.-F.,Zhengzhou University | Hao S.-G.,Henan University of Science and Technology | Hao S.-G.,Xinxiang Center Hospital | And 3 more authors.
Experimental and Therapeutic Medicine | Year: 2013

The aim of this study was to characterize histochemical patterns and Das-1 and Ki67 protein expression in gastric cardia adenocarcinoma (GCA) and intestinal metaplasia (IM) lesions adjacent to GCA. Histochemical techniques, including Alcian blue/periodic acid-Schiff (AB/PAS), high iron diamine/Alcian blue (HID/AB) and avidin-biotin-peroxidase complex (ABC) immunohistochemistry were applied to GCA and IM samples from patients (n=200) in Linzhou, Henan, China, a high incidence area for GCA and esophageal squamous cell carcinoma (SCC). The detection rate of IM lesions in resected tissues adjacent to GCA was 32.5% (65/200). GCA and IM lesions presented a high frequency of Das-1 and Ki67-positive staining with statistical significance (P<0.01). The expression of sulfuric proteins did not show co-expression with Das-1 and Ki67 in GCA and surrounding IM lesions (P>0.05) from the same GCA patient. The high frequency of co-expression of Das-1 and Ki67 in GCA and adjacent IM lesions indicates that IM adjacent to GCA may undergo similar molecular changes to GCA, which may be one of the mechanisms for malignant transformation of IM in the population studied.

Li C.-Y.,Xinxiang Center Hospital | Zhang H.-Y.,Xinxiang Center Hospital | Gao Y.-L.,Nantong University
Molecular Medicine Reports | Year: 2014

Glioma is the most common brain malignancy and has a very poor prognosis. The current treatment options have a minimal benefit on prolonging patient survival time. Accumulating data have shown that the WNT signaling pathway has a critical function in the progression and invasion of glioma. Thus, targeting WNT signaling appears to be an effective anti-glioma strategy. TIKI2 was recently found to suppress the activation of the WNT signaling pathway by post-translationally modifying secreted WNT proteins. The implication of TIKI2 aberrance in cancers and its potential therapeutic effect, however, has not been studied. In the present study, a glioma-specific adenoviral vector was constructed, which was regulated by response elements of miR-124, to express TIKI2 in glioma cells (Ad-TIKI2-124). Ad-TIKI2-124 was found to potently suppress the activation of WNT signaling in glioma cells. This inhibitory effect on the WNT signaling pathway lead to the reduction in proliferation, colony formation ability and invasion of glioma cell lines. In addition, animal experiments confirmed that the expression of the Ad-TIKI2-124 construct could compromise the tumorigenicity of glioma cells in vivo. Furthermore, this glioma-selective TIKI2 expression protected normal cells from toxicity. In conclusion, the present study demonstrated that adenovirus-mediated TIKI2 therapy may be used for glioma treatment and therefore warrants further clinical studies.

Liu G.,Guangxi Medical University | Liu G.,Xinxiang Center Hospital | Wu D.,Guangxi Medical University | Wu D.,Xinxiang Center Hospital | And 3 more authors.
Oncology Reports | Year: 2015

Nasopharyngeal carcinoma (NPC) is the most commonly diagnosed head and neck malignancy and is prevalent worldwide. Previous studies have demonstrated the antitumor properties of cepharanthine hydrochloride (CH) in several human cancer cells. However, the action of CH in NPC cells has yet to be determined. In the present study, we investigated the effects of CH in human NPC cell lines including CNE-1 and CNE-2 on cell growth and apoptosis in vitro. Using MTT and ATP-tumor chemosensitivity assays it was found that CH inhibited cell viability. Additionally, flow cytometric and analysis electron microscopy revealed the inhibition of cell cycle progression and reduction of apoptosis, respectively, in human NPC cell lines including CNE-1 and CNE-2 in vitro. To identify the potential action mechanisms of CH, the cDNA microarray analysis results were confirmed by quantitative PCR analysis using a number of genes, including CDKN1A/P21, NR4A1/TR3 and DAXX. In total, 138 upregulated and 63 downregulated genes in CNE-2 cells were treated with CH. According to their biological function, the genes were classified as: i) cell cycle-related genes; ii) DNA repair-related genes; iii) apoptosis-related genes and iv) nuclear factor-κB (NF-κB) transcription factors signal pathways. The results of the present study showed that CH is a potential therapeutic agent against human NPC, and provide rational explanations and a scientific basis for the study of the development of CH in the treatment of NPC.

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