Second Peoples Hospital of Nantong

Nantong, China

Second Peoples Hospital of Nantong

Nantong, China
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Ge J.-B.,Second Peoples Hospital of Nantong | Ge J.-B.,Soochow University of China | Lu H.-J.,Second Peoples Hospital of Nantong | Song X.-J.,Second Peoples Hospital of Nantong | And 3 more authors.
Zhongguo Zhongyao Zazhi | Year: 2017

To observe the protective effects of Lycium barbarum polysaccharides (LBP) on cerebral ischemia reperfusion injury in mice and explore its mechanism. Common carotid artery thread was used to cause middle cerebral artery ischemia, And the thread was taken out after 2 h ischemia to achieve cerebral ischemia reperfusion injury in mice. Therefore, The transient middle cerebral artery occlusion (tMCAO) models were established to observe the effects of LBP (25, 50, 100 mg · Kg-1) on neurological outcome, Infarct size and water contents. HE staining was used to observe its effects on neurocytes of cerebral tissues in mice. Western blotting was used to evaluate the protein expression levels of NF-κB p65. ELISA was used to evaluate the levels of TNF-α, IL-6 and IL-1β In the serum. According to the results, LBP markedly improved neurologic deficits, And decreased infarct size and water contents at 24 h after reperfusion in mice. Pathological section of brain tissues also proved its protective effects on neurocytes. Western blot analysis indicated that LBP markedly down-regulated the protein level of NF-κB p65. ELISA indicated that LBP decreased the levels of TNF-α, IL-6 and IL-1β in the serum 24 h after reperfusion. In conclusion, LBP has protective effects on cerebral ischemia reperfusion injury in mice, and this effect may be associated with inhibiting NF-κB and inflammatory reactions.

Gu G.,Nantong University | Chen Y.,Nantong University | Duan C.,Second Peoples Hospital of Nantong | Zhou L.,Nantong University | And 7 more authors.
Oncology Reports | Year: 2017

ADP-ribosylation factor 1 (ARF1) is a small G protein that regulates many cellular processes such as reorganization of the actin cytoskeleton and is highly expressed in various tumor cells and tissues. However, the role of ARF1 in ovarian cancer progression remains unknown. In the present study, we explored the expression patterns of ARF1 in clinical ovarian cancer samples and adjacent noncancerous tissues. The results revealed that ARF1 overexpressed in EOC tissues and cell lines, compared with the adjacent non-tumorous tissues and normal ovarian cells. In addition, the immunoreactivity of ARF1 was positively correlated with EOC grade and Ki-67 expression. Knockdown of ARF1 expression notably inhibited cell proliferation and migration rate of EOC cells by the auxiliary of PI3K. Taken together, our findings provide new insights into the functional role of ARF1 on EOC cell growth and migration and it may serve as a diagnostic and therapeutic target.

Ge J.-B.,Soochow University of China | Ge J.-B.,Second Peoples Hospital of Nantong | Gu J.-H.,Soochow University of China | Gu J.-H.,Nantong University | And 4 more authors.
Chinese Pharmacological Bulletin | Year: 2012

Aim: To observe the protective effects of Ginkgolide A (GA) on cerebral ischemia-reperfusion injury in mice and explore its mechanism. Methods: Cerebral ischemia-reperfusion injury in mice was induced by middle cerebral artery occlusion. The neurological outcome, infarct size and water contents were evaluated. The pathomorphology examination was done. Western blot analysis was employed to determine alterations in protein levels of IκBα, pIκBα and Caspase-3. Quantitative Real-Time RT-PCR was used to detect induction of NF-κB target gene p53 mRNA. Results: GA(40, 20 mg·kg -1) markedly improved neurologic deficits, and decreased infarct volume and edema at 24 h after reperfusion in mice. The pathological slices also proved its protective effects on neuron cells. Western blot analysis indicated a significant decrease in IκBα levels after ischemia. GA markedly up-regulated the protein levels of IκBα, and down-regulated the protein levels of pIκBα and Caspase-3. GA also repressed the ischemia-induced increase in expression of NF-κB target gene p53 mRNA. Conclusion: GA has protective effects on cerebral ischemia-reperfusion injury in mice. Which is probably related to inhibition of NF-κB signaling pathway and down-regulation of the levels of p53 and Caspase-3.

Qin X.-F.,Fudan University | Lu X.-J.,Nantong University | Ge J.-B.,Second Peoples Hospital of Nantong | Xu H.-Z.,Fudan University | And 2 more authors.
NeuroReport | Year: 2014

Ginkgolide B (GB) has been shown to exert neuroprotective effects against cerebral ischemia/reperfusion (I/R) injury. However, the underlying mechanism by which GB prevents ischemic cell death remains unclear. Lysosomal proteases, including cathepsins B and L, have been implicated in ischemic cell death following reperfusion. Therefore, in the present study, we investigated the role of GB with respect to cathepsin-mediated cell death following I/R. Both the expression and enzymatic activity of cathepsins B and L were significantly increased in the ischemic cortex following cerebral I/R injury. We found that GB treatment markedly decreased the activity and expression of cathepsins B and L following I/R. Moreover, GB reduced necrotic and apoptotic cell death following I/R. These data strongly suggest that GB prevents cathepsin-mediated cell death following focal cerebral I/R injury, and they might provide new insights into the mechanism of the neuroprotective effects of GB.

Gu J.-H.,Soochow University of China | Gu J.-H.,Nantong University | Ge J.-B.,Soochow University of China | Ge J.-B.,Second Peoples Hospital of Nantong | And 5 more authors.
European Journal of Pharmaceutical Sciences | Year: 2012

Ginkgolide B (GB) has potent neuroprotective effects against ischemia-induced brain injury in vivo and in vitro. However, the underlying mechanisms of GB's neuroprotection remain poorly understood. Excessive inflammation and apoptosis contribute to the pathogenesis of ischemic brain damage, and NF-κB is considered to be a key player in these processes. In the present study, we examined the detailed mechanisms underlying the inhibitory effects of GB on inflammatory and apoptotic responses induced by focal cerebral ischemia/reperfusion (I/R). Transient middle cerebral artery occlusion (tMCAO) model was produced by using an intraluminal filament technique in mice. GB (10, 20 and 40 mg/kg) was administered intravenously (i.v.) 2 h after MCAO. The results demonstrated that MCAO-induced cerebral injury was associated with an upregulation of p-IKK, p-IκB-α and degradation of IκB-α, indicating of NF-κB activation. Meanwhile activation of microglial and increases in levels of TNF-α, IL-1β and iNOS were observed. Furthermore upregulation of the expression of NF-κB target gene p53 and p53 downstream gene Bax, but downregulation of Bcl-2 and activation of caspase-3 were found. GB treatment showed marked reduction in infarction volume, brain edema and neurological deficits. GB also inhibited I/R induced NF-κB, microglia activation and production of pro-inflammatory cytokines. We also demonstrated that GB reduced Bax protein levels and increased Bcl-2 protein levels in the post-ischemic brains. These results suggest that GB's neuroprotection is attributable to its anti-inflammatory and anti-apoptotic effect through inhibition of NF-κB. © 2012 Elsevier B.V. All rights reserved.

Wu F.,Soochow University of China | Wu F.,Nantong University | Wang Z.,Soochow University of China | Gu J.-H.,Soochow University of China | And 4 more authors.
Neurochemistry International | Year: 2013

Rotenone is an environmental neurotoxin that induces degeneration of dopaminergic (DA) neurons in substantia nigra pars compacta (SNpc), which ultimately results in parkinsonism, but the molecular mechanisms of selective degeneration of nigral DA neurons are not fully understood. In the present study, we investigated the induction of p38MAPK/p53 and Bax in SNpc of Lewis rats after chronic treatment with rotenone and the contribution of Bax to rotenone-induced apoptotic commitment of differentiated PC12 cells. Lewis rats were subcutaneously treated with rotenone (1.5 mg/kg) twice a day for 50 days and the loss of tyrosine hydroxylase (THase), motor function impairment, and expression of p38MAPK, P-p38MAPK, p53, and Bax were assessed. After differentiated PC cells were treated with rotenone (500 nM) for 6-36 h, protein levels of p38MAPK and P-p38MAPK, p53 nuclear translocation, Bax induction and cell death were measured. The results showed that rotenone administration significantly reduced motor activity and caused a loss of THase immunoreactivity in SNpc of Lewis rats. The degeneration of nigral DA neurons was accompanied by the increases in p38MAPK, P-p38MAPK, p53, and Bax protein levels. In cultured PC12 cells, rotenone also induced an upregulation of p38MAPK, P-p38 MAPK, p53 and Bax. Pharmacological inhibition of p38MAPK with SB203580 (25 μM) blunted rotenone-induced cell apoptosis. Treatment with SB203580 prevented the p53 nuclear translocation and upregulation of Bax. Inhibition of p53 with pifthrin-alpha or Bax with siRNAs significantly reduced rotenone-induced Bax induction and apoptotic cell death. These results suggest that the p38MAPK/p53-dependent induction of Bax contributes to rotenone's neurotoxicity in PD models. © 2013 Elsevier Ltd. All rights reserved.

Gu J.,Nanjing Medical University | Shi W.,Second Peoples Hospital of Nantong | Lu Y.,Nanjing Medical University | Zhu Q.,Nanjing Medical University | And 5 more authors.
International Immunopharmacology | Year: 2015

Graft-versus-host disease (GVHD) is an intractable complication in transplant patients. Regulatory T cells (Tregs) have the ability to prevent GVHD and consist of two subsets: natural Tregs (nTregs) and induced Tregs (iTregs). In comparison to nTregs, iTregs originate in the periphery under certain conditions and show improved proliferative and suppressive abilities in an inflammatory milieu. All-trans retinoic acid (atRA) favors Treg expansion and FoxP3 expression in human Tregs. However, whether atRA can affect the function of iTregs from transplant patients remains inconclusive. Therefore, we sorted naïve T cells from liver transplant patients and cultured them in vitro. Further analyses were performed to assess the suppressive function of iTregs in vitro and in vivo. atRA favored expansion and forkhead box P3 expression in iTregs from transplant patients. In comparison to iTregs from healthy donors, iTregs from transplant patients showed decent suppressive abilities in vitro and in vivo. Our findings suggest that atRA can potentially improve the development and function of iTregs from transplant patients. Furthermore, our results provide novel insights into Treg therapy in GVHD clinical trials. © 2015 Elsevier B.V.

Shi W.,Nanjing Medical University | Shi W.,Key Laboratory of Living Donor Liver Transplantation | Shi W.,Second Peoples Hospital of Nantong | Zhu Q.,Nanjing Medical University | And 10 more authors.
Clinical and Developmental Immunology | Year: 2013

To investigate the relationship between interleukin-17 and proteins involved in fatty acid metabolism with respect to alcoholic liver disease, male ICR mice were randomized into five groups: control, alcoholic liver disease (ALD) at 4 weeks, 8 weeks, and 12 weeks, and anti-IL-17 antibody treated ALD. A proteomic approach was adopted to investigate changes in liver proteins between control and ALD groups. The proteomic analysis was performed by two-dimensional difference gel electrophoresis. Spots of interest were subsequently subjected to nanospray ionization tandem mass spectrometry (MS/MS) for protein identification. Additionally, expression levels of selected proteins were confirmed by western blot. Transcriptional levels of some selected proteins were determined by RT-PCR. Expression levels of 95 protein spots changed significantly (ratio >1.5, P<0.05) during the development of ALD. Sterol regulatory element-binding protein-lc (SREBP-1c), carbohydrate response element binding protein (ChREBP), enoyl-coenzyme A hydratase (ECHS1), and peroxisome proliferator-activated receptor alpha (PPAR-α) were identified by MS/MS among the proteins shown to vary the most; increased IL-17 elevated the transcription of SREBP-1c and ChREBP but suppressed ECHS1 and PPAR-α. The interleukin-17 signaling pathway is involved in ALD development; anti-IL-17 antibody improved hepatic steatosis by suppressing interleukin-17-related fatty acid metabolism. © 2013 Weidong Shi et al.

Sun X.,Second Peoples Hospital of Nantong | Huang X.,Second Peoples Hospital of Nantong | Zhao R.,Second Peoples Hospital of Nantong | Chen B.,Second Peoples Hospital of Nantong | Xie Q.,Second Peoples Hospital of Nantong
Pancreatology | Year: 2015

Background and aim Questions remain unclear about the association of smoking status and the development of acute pancreatitis (AP). We performed a meta-analysis of observational studies explore this association. Methods A computerized literature search was performed in MEDLINE and EMBASE through November 30, 2014. We also searched the reference lists of pertinent articles. We used a random-effects model to calculate the summary relative risks (SRRs) and their corresponding 95% confidence intervals (CIs). Results A total of 3690 incident cases of AP included 12 observational studies (6 case-control and 6 prospective cohort/nested case-control studies) were identified. Compared with never smokers, the summary RR estimates were 1.54 (95% CI, 1.31-1.80) for ever smokers, 1.71 (95% CI, 1.37-2.14) for current smokers, and 1.21 (95% CI, 1.02-1.43) for former smokers. Smoking is found to be a potential risk factor for alcohol use, idiopathic factors and drugs related AP, but not for gallstone related AP, in the ever and current smokers. A dose-response effect of tobacco use on the risk was ascertained: current smokers had a 40% (95% CI, 30%-51%) increased risk of AP for every additional 10 cigarettes per day. Conclusion The present analysis suggests that smokers have an elevated risk of AP development. Further studies, however, are warranted before definitive conclusions can be drawn. © 2015 IAP and EPC.

Ge J.-F.,Second Peoples Hospital of Nantong | Cao S.-F.,Second Peoples Hospital of Nantong
Journal of Clinical Dermatology | Year: 2014

Objective: To summarize the experience of diagnosis and treatment of scrub typhus, and to reduce the rate of misdiagnosis and missed diagnosis. Methods: The medical records of 15 inpatients from November 2010 to December 2011 were analyzed. Results; All patients had different degrees of fever, some patients had liver, lung or kidney damages; 14 cases had typical eschar or specific ulcer. Treatment with doxycycline obtained good results. Conclusion; Scrub typhus is of various clinical manifestations, detailed medical history investigation and physical examination are very important in reducing misdiagnosis and missed diagnosis. Doxycycline and azithromycin are effective drugs for treating scrub typhus.

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