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Wan H.,Shanghai Minhang District Central Hospital | Yuan Y.,Shanghai JiaoTong University | Liu J.,Shanghai Minhang District Central Hospital | Chen G.,Shanghai Songjiang District Central Hospital
Translational Research | Year: 2012

The purpose of this study was to test the hypothesis that activation of endogenous peroxisome proliferator-activated receptor (PPARγ) inhibits induction of early growth response factor-1 (Egr-1), which is rapidly induced in the pancreas following cerulein intraperitoneal injection. Acute pancreatitis was induced in mice by hourly intraperitoneal injection of cerulein. Pioglitazone was administered prophylactically and pancreatic inflammation was assessed. AR42J cells were stimulated with caerulein10 -8M co-incubated in presence of different concentration of pioglitazone. The expression of PPARγ, Egr-1, and the target genes of Egr-1 were studied by real-time reverse transcriptase polymerase chain reaction (PCR), Western blot, and immunohistochemistry. In vitro, a PPAR-γ activator (pioglitazone) strikingly diminished Egr-1 mRNA and protein expression corresponding to Egr-1. In vivo, treatment with pioglitazone prior to the intraperitoneal injection of cerulein induction of Egr-1 and its target genes such as, monocyte chemotactic protein-1 (MCP-1) and macrophage inflammatory protein-1 (MIP-1). The inhibitory effect of pioglitazone on Egr-1 expression induced by cerulein was almost fully restored by GW9662. Activation of PPAR-γ suppressed the activation of Egr-1 and its inflammatory gene targets and provided potent protection against pancreas injury. These data suggest a new mechanism in which PPAR-γ activation may decrease tissue inflammation in response to a cerulein insult. © 2012 Mosby, Inc. All rights reserved.

Wan H.,Shanghai Songjiang District Central Hospital | Chen Y.,Zhengzhou University
International Journal of Psychiatry in Medicine | Year: 2010

Background and Aim: Irritable bowel syndrome (IBS) patients usually manifest autonomic nerve dysfunctions and abnormal psychological behaviors. This study was to assess autonomic nervous system (ANS) response to different stressor as well as evaluate effects of antidepressive treatment of Saint John's Wort Extract in women with IBS. Method: Thirty women with IBS and 20 healthy women underwent serial ANS function tests. Five-minute-short-time heart rate variability (HRV) spectral analysis were assessed at a stress or resting recording period. Hamilton Depression Scale (HAMD) and Hamilton Anxiety Scale (HAMA) were used to measure their anxiety and depression conditions. After 8-weeks' antidepressant treatment, groups of IBS repeated the tests above. Subjects also completed a GI symptom diary once daily during the 2 weeks before therapy and for 2 weeks in the last scheduled therapy session. Results: IBS-group showed a higher score in HAMA and HAMD (p < 0.01) and showed a significant increase in the low frequency band/high frequency band ratio (L/H) during the period in different stimuli (p < 0.01), which was significantly different from controls. After 8-weeks' antidepressive treatment, L/H showed a significant decrease (p < 0.05) response to different stressor, which was significantly different from pre-treatment. Gastrointestinal (GI) symptoms of IBS were also relieved significantly. Conclusions: Antidepressive treatment can improve the conditions of psychology and the ANS reactivity to stress in patients with IBS. © 2010, Baywood Publishing Co., Inc.

Yu M.,Fudan University | Chen X.,Hainan Provincial Nong Ken Hospital | Lv C.,Fudan University | Yi X.,Shanghai Songjiang District Central Hospital | And 5 more authors.
Biochemical and Biophysical Research Communications | Year: 2014

Osteoclasts, derived from hemopoietic progenitors of the monocyte/macrophage lineage, have a unique role in bone resorption, and are considered a potential therapeutic target in the treatment of such pathologic bone diseases as osteoporosis, rheumatoid arthritis, and periodontitis. In the present study, we demonstrate that curcumol, one of the major components of the essential oil of Rhizoma Curcumae, exhibits an inhibitory effect on receptor activator of nuclear factor kappaB ligand (RANKL)-induced osteoclast differentiation with both bone marrow-derived macrophages and RAW264.7 cells in a dose-dependent manner. In addition, RANKL-induced mRNA expression of osteoclast-specific genes, such as tartrate-resistant acid phosphatase, calcitonin receptor, and cathepsin K, is prominently reduced in the presence of curcumol. Furthermore, the molecular mechanism of action was investigated, and curcumol inhibited osteoclastogenesis by specifically impairing RANKL-induced c-Jun N-terminal kinase (JNK)/activator protein-1 (AP-1) signaling, which was further identified in rescue studies by means of anisomycin, a JNK signaling-specific activator. Taken together, these findings suggest that curcumol suppresses RANKL-induced osteoclast differentiation through the JNK/AP-1 signaling pathway, and may be useful as a therapeutic treatment for bone resorption-associated diseases. © 2014 Elsevier Inc. All rights reserved.

Wang Y.,Jiangsu University | Wang Y.,Shanghai JiaoTong University | Li J.,Shanghai JiaoTong University | Wen S.,Shanghai Songjiang District Central Hospital | And 4 more authors.
American Journal of Translational Research | Year: 2015

Endometrial carcinoma is the most common gynecologic malignancy. Searching for a new molecule to more accurately predict survival of patients and act as therapy target is urgent. CHRM3 is a major player in many kinds of cancer. The expression level and prognostic value of CHRM3 in endometrial carcinoma remain unclear. In this study, we assayed the expression of CHRM3 in 257 endometrial carcinoma patients by immunohistochemistry. The results showed that CHRM3 expression level was closely correlated with the FIGO stage, vascular invasion and lymphatic metastasis. Although CHRM3 was highly expressed in advanced endometrial carcinoma, multivariate Cox proportional hazards regression analysis showed that CHRM3 expression was not an independent prognostic factor for endometrial carcinoma. Furthermore, to evaluate the prognostic efficiency of CHRM3 in endometrial carcinoma, we compared the sensitivity and specificity of CHRM3 in endometrial carcinoma prognosis by logistic regression. The result showed that CHRM3 combining with other clinicopathological risk factors was a stronger prognostic model than clinicopathological risk factor alone or combination of risk factors. Thus, CHRM3 potentially offers a clinical value in target therapy for endometrial carcinoma patients. © 2015, E-Century Publishing Corporation. All Rights Reserved.

Wen S.-Y.,Shanghai JiaoTong University | Lin Y.,Shanghai JiaoTong University | Yu Y.-Q.,Shenyang Medical College | Cao S.-J.,Shanghai Songjiang District Central Hospital | And 11 more authors.
Oncogene | Year: 2014

Although significant advances have recently been made in the diagnosis and treatment of cervical carcinoma, the long-term survival rate for advanced cervical cancer remains low. Therefore, an urgent need exists to both uncover the molecular mechanisms and identify potential therapeutic targets for the treatment of cervical cancer. MicroRNAs (miRNAs) have important roles in cancer progression and could be used as either potential therapeutic agents or targets. miR-506 is a component of an X chromosome-linked miRNA cluster. The biological functions of miR-506 have not been well established. In this study, we found that miR-506 expression was downregulated in approximately 80% of the cervical cancer samples examined and inversely correlated with the expression of Ki-67, a marker of cell proliferation. Gain-of-function and loss-of-function studies in human cervical cancer, Caski and SiHa cells, demonstrated that miR-506 acts as a tumor suppressor by inhibiting cervical cancer growth in vitro and in vivo. Further studies showed that miR-506 induced cell cycle arrest at the G1/S transition, and enhanced apoptosis and chemosensitivity of cervical cancer cell. We subsequently identified Gli3, a hedgehog pathway transcription factor, as a direct target of miR-506 in cervical cancer. Furthermore, Gli3 silencing recapitulated the effects of miR-506, and reintroduction of Gli3 abrogated miR-506-induced cell growth arrest and apoptosis. Taken together, we conclude that miR-506 exerts its anti-proliferative function by directly targeting Gli3. This newly identified miR-506/Gli3 axis provides further insight into the pathogenesis of cervical cancer and indicates a potential novel therapeutic agent for the treatment of cervical cancer.Oncogene advance online publication, 10 March 2014; doi:10.1038/onc.2014.9.

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