No323 Hospital Of Pla

Fengcheng, China

No323 Hospital Of Pla

Fengcheng, China

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Zhao Y.-L.,No323 Hospital Of Pla | Song H.-R.,No323 Hospital Of Pla | Fei J.-X.,No323 Hospital Of Pla | Liang Y.,PLA Fourth Military Medical University | And 4 more authors.
Journal of Traditional Chinese Medicine | Year: 2012

OBJECTIVE: To examine the clinical effects of a mixture of Chinese Yam and Epimedium in patients with stable moderate or severe chronic obstructive pulmonary disease (COPD). METHODS: Forty-nine patients with COPD were randomly allocated to a group whose usual treatment was supplemented with oral Chinese Yam-Epimedium mixture, or a control group given placebo. For each patient, body mass index, airflow obstruction, dyspnea, and exercise capacity were measured and converted into the BODE index before treatment and at one and three months after initiation of treatment. Participants also completed the St George's Respiratory Questionnaire (SGRQ) at the same intervals. RESULTS: After one month, improvements were seen in the BODE index and SGRQ of participants taking Chinese Yam-Epimedium mixture compared to controls. There were statistically significant differences in the SGRQ: three of its components and the total SGRQ scores were significantly decreased (P<0.05), respiratory symptom scores had improved (P<0.01), and the dyspnea component of the BODE index had significantly decreased (P<0.05). Similar improvements were observed after three months of treatment, but exercise tolerance had also improved: the six-minute walking distance had significantly increased (P<0.05) in the treatment group when compared with controls. CONCLUSION: Chinese Yam-Epimedium mixture can significantly improve dyspnea, exercise capacity, and the quality of life of patients with stable moderate or severe COPD. © 2012 JTCM. All rights reserved.


Yu L.,PLA Fourth Military Medical University | Yu L.,3rd Hospital of PLA | Su Y.-S.,PLA Fourth Military Medical University | Su Y.-S.,No323 Hospital Of Pla | And 3 more authors.
FEBS Letters | Year: 2013

Epigenetic silencing mechanisms play an important role in chemoresistance of human cancer. Here we report the upregulated expression of metastasis-associated protein 1 (MTA1), a component of the nucleosome remodeling deacetylation (NuRD) complex, in chemoresistant prostate cancer (PCa). MTA1 knockdown in PC-3 cells inhibited cell proliferation and enhanced docetaxel (DTX)-induced cell death. Conversely, overexpression of MTA1 promotes DTX chemoresistance in PC-3 cells. MTA1 acted as a potent corepressor of the nuclear receptor NR4A1 transcription by interacting with histone deacetylase 2 (HDAC2). These findings suggest that MTA1 may serve as a novel DTX-resistance promoter in PC-3 cells. © 2013 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.


Li B.,No323 Hospital Of Pla | Bai W.,No323 Hospital Of Pla | Sun P.,No323 Hospital Of Pla | Zhou B.,No323 Hospital Of Pla | And 2 more authors.
Journal of Interferon and Cytokine Research | Year: 2015

Endothelial progenitor cells (EPCs) may contribute to vascular repair and angiogenesis. Chemokine (C-X-C motif) ligand 12 (CXCL12/SDF-1) is known to play an important role in the mobilization and recruitment of progenitor cells. Therefore, we assessed the function of CXCL12 as a stimulating molecule of angiogenesis in EPCs and the underlying mechanism after intracerebral hemorrhage (ICH). Isolated EPCs from male Sprague-Dawley rats, stimulate with various doses of CXCL12. Then, 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay was used to assess the proliferation of EPCs, and cell migration and adhesion were analyzed by transwell chamber assay. Furthermore, mRNA levels of endothelial markers von Willebrand Factor (vWF), Tie-2, and vascular endothelial cadherin (VE-cadherin) were explored by real-time polymerase chain reaction. Capillary tube and vessel formation in vitro and in vivo were detected after pretreatment with the C-X-C chemokine receptor type 4 (CXCR4) inhibitor AMD3100. Following stimulation with various doses of CXCL12, an obvious dose-dependent increase in the proliferation, migration, and adhesion of EPCs was confirmed. Furthermore, the mRNA levels of endothelial markers vWF, Tie-2, and VE-cadherin were also demonstrated in CXCL12-treated EPCs, indicating that CXCL12 could regulate EPC differentiation to endothelial cells. Importantly, these increases depended on the activation of CXCR4 signaling, as pretreatment with CXCR4 inhibitor AMD3100 dramatically dampened the CXCL12-induced effects. Additionally, blocking CXCR4 signaling dampened CXCL12-induced angiogenic activity both in vitro and in vivo. Following construction of a rodent ICH model, scaffolds delivering CXCL12 together with EPCs resulted in an evident increase in blood vessel formation; however, this increase in blood vessels was attenuated with delivery of AMD3100. CXCL12 stimulates EPCs to induce angiogenesis though the CXCR4 pathway after ICH. Consequently, our findings provide a potential target for angiogenesis in ICH. © 2015, Mary Ann Liebert, Inc.


PubMed | No323 Hospital Of Pla
Type: Journal Article | Journal: Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research | Year: 2015

Endothelial progenitor cells (EPCs) may contribute to vascular repair and angiogenesis. Chemokine (C-X-C motif) ligand 12 (CXCL12/SDF-1) is known to play an important role in the mobilization and recruitment of progenitor cells. Therefore, we assessed the function of CXCL12 as a stimulating molecule of angiogenesis in EPCs and the underlying mechanism after intracerebral hemorrhage (ICH). Isolated EPCs from male Sprague-Dawley rats, stimulate with various doses of CXCL12. Then, 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay was used to assess the proliferation of EPCs, and cell migration and adhesion were analyzed by transwell chamber assay. Furthermore, mRNA levels of endothelial markers von Willebrand Factor (vWF), Tie-2, and vascular endothelial cadherin (VE-cadherin) were explored by real-time polymerase chain reaction. Capillary tube and vessel formation in vitro and in vivo were detected after pretreatment with the C-X-C chemokine receptor type 4 (CXCR4) inhibitor AMD3100. Following stimulation with various doses of CXCL12, an obvious dose-dependent increase in the proliferation, migration, and adhesion of EPCs was confirmed. Furthermore, the mRNA levels of endothelial markers vWF, Tie-2, and VE-cadherin were also demonstrated in CXCL12-treated EPCs, indicating that CXCL12 could regulate EPC differentiation to endothelial cells. Importantly, these increases depended on the activation of CXCR4 signaling, as pretreatment with CXCR4 inhibitor AMD3100 dramatically dampened the CXCL12-induced effects. Additionally, blocking CXCR4 signaling dampened CXCL12-induced angiogenic activity both in vitro and in vivo. Following construction of a rodent ICH model, scaffolds delivering CXCL12 together with EPCs resulted in an evident increase in blood vessel formation; however, this increase in blood vessels was attenuated with delivery of AMD3100. CXCL12 stimulates EPCs to induce angiogenesis though the CXCR4 pathway after ICH. Consequently, our findings provide a potential target for angiogenesis in ICH.

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