Bethune International Peace Hospital of Chinese PLA

Hebei, China

Bethune International Peace Hospital of Chinese PLA

Hebei, China
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Wang X.,Hebei Medical University | Wu H.,Bethune International Peace Hospital of Chinese PLA | Xue G.,Bethune International Peace Hospital of Chinese PLA | Hou Y.,Hebei Medical University | Hou Y.,Bethune International Peace Hospital of Chinese PLA
Neural Regeneration Research | Year: 2012

In this study, human umbilical cord mesenchymal stem cells from full-term neonates born by vaginal delivery were cultured in medium containing 150 mg/mL of brain tissue extracts from Sprague-Dawley rats (to mimic the brain microenvironment). Immunocytochemical analysis demonstrated that the cells differentiated into neuron-like cells. To evaluate the effects of progesterone as a neurosteroid on the neuronal differentiation of human umbilical cord mesenchymal stem cells, we cultured the cells in medium containing progesterone (0.1, 1, 10 μM) in addition to brain tissue extracts. Reverse transcription-PCR and flow cytometric analysis of neuron specific enolase-positive cells revealed that the percentages of these cells increased significantly following progesterone treatment, with the optimal progesterone concentration for neuron-like differentiation being 1 μM. These results suggest that progesterone can enhance the neuronal differentiation of human umbilical cord mesenchymal stem cells in culture medium containing brain tissue extracts to mimic the brain microenvironment. © 2012, Editorial Board of Neural Regeneration Research. All rights reserved.

Li J.-L.,Hebei General Hospital | Gao D.-Y.,Hebei General Hospital | Du Y.-R.,Hebei General Hospital | Hou Y.-N.,Bethune International Peace Hospital of Chinese PLA
Chinese Pharmacological Bulletin | Year: 2014

Aim: To investigate the effects of 17β-estradiol on the apoptosis induced by ketamine in primary cultured cortical neurons. Methods: Primary cultured cortical neurons were treated with different concentrations of ketamine or 17β-estradiol respectively. 24 hours after various treatments, neuron viability was measured by MTT assay. The structure of neurons was analyzed using microscope. Apoptotic neurons were determined by the TUNEL assay. The level of pAkt expression was analyzed by Western blot. Results: Compared with the control group, ketamine decreased neuron viability in a dose-dependent manner. Compared with ketamine group, 17β-estradiol increased neuron viability in a dose-dependent manner. Lack of three-dimensional sense, faded color, uncleared outline were observed, and fractured neuron axons or neurons death were also observed in neurons treated by 100 μmol·L-1 ketamine. 100 μmol·L-1 ketamine increased the number of apoptotic neurons and decreased the expression of pAkt. 0.1 μmol·L -117β-estradiol decreased the number of apoptotic neurons and increased the expression of pAkt. LY294002 inhibited the protective effects of 17β-estradiol, the number of apoptotic neurons increased, and the level of pAkt decreased significantly. Conclusion: 17β-estradiol exerts the neuroprotective effects against ketamine-induced neuroapoptosis by activating the PI3K/Akt signaling pathway.

Liu S.,Hebei Medical University | Wu H.H.,Bethune International Peace Hospital of Chinese PLA | Xue G.,Bethune International Peace Hospital of Chinese PLA | Ma X.,Hebei Medical University | And 4 more authors.
Neural Regeneration Research | Year: 2013

A correlation between metabolic alterations of neuroactive steroids and Alzheimer's disease remains unknown. In the present study, amyloid beta (Aβ) 25-35 (Aβ25-35) injected into the bilateral campus CA1 region significantly reduced learning and memory. At the biochemical level, hippocampal levels of pregnenolone were significantly reduced with Aβ25-35 treatment. Furthermore, progesterone was considerably decreased in the prefrontal cortex and hippocampus, and 17β-estradiol was significantly elevated. To our knowledge, this is the first report showing that Aβ25-35, a main etiological factor of Alzheimer's disease, can alter the level and metabolism of neuroactive steroids in the prefrontal cortex and hippocampus, which are brain regions significantly involved in learning and memory. Aβ25-35 exposure also increased the expression of inflammatory mediators, tumor necrosis factor-α and interleukin-1β. However, subcutaneous injection of progesterone reversed the upregulation of tumor necrosis factor-α and interleukin-1β in a dose-dependent manner. Concomitant with improved cognitive abilities, progesterone blocked Aβ-mediated inflammation and increased the survival rate of hippocampal pyramidal cells. We thus hypothesize that Aβ-mediated cognitive deficits may occur via changes in neuroactive steroids. Moreover, our findings provide a possible therapeutic strategy for Alzheimer's disease via neuroactive steroids, particularly progesterone.

Li B.-S.,Chinese PLA Medical School | Sun D.-X.,Chinese PLA Medical School | Sun D.-X.,Bethune International Peace Hospital of Chinese PLA
World Chinese Journal of Digestology | Year: 2016

During hepatitis B virus (HBV) infection, covalently closed circular DNA (cccDNA) acts as the template for the synthesis of viral RNA and new virions. Current therapies rarely achieve an elimination of cccDNA. Biosynthesis of relaxed circular (RC) DNA by reverse transcription of the viral pregenomic RNA is now understood quite well, yet conversion of RC-DNA to cccDNA is still obscure. Conceptual and recent experimental data link cccDNA formation to cellular DNA repair, which is increasingly appreciated as a critical interface between cells and viruses. This review aims to summarize current knowledge on cccDNA molecular biology, to highlight the experimental restrictions that have hitherto hampered faster progress and to discuss cccDNA as a target for potentially curative therapies for chronic hepatitis B. © 2016 Baishideng Publishing Group Inc. All rights reserved.

Li J.,Hebei Medical University | Li J.,Hebei General Hospital | Wu H.,Bethune International Peace Hospital of Chinese PLA | Xue G.,Bethune International Peace Hospital of Chinese PLA | And 3 more authors.
Basic and Clinical Pharmacology and Toxicology | Year: 2013

Numerous studies in rodents have indicated that exposure to ketamine during the period when synaptogenesis is highly active induces neurodegeneration. Thus, there is a growing need to develop strategies to prevent ketamine-induced brain injury in the developing brain. Oestradiol is a neuroactive steroid that prevents neuronal cell death in different experimental models by activating cell survival signals and inhibiting apoptotic signals. The main goal of this study was to investigate the neuroprotective effects of 17β-oestradiol against ketamine-induced apoptotic neurodegeneration in primary-cultured cortical neurons. The data revealed that 17β-oestradiol (0.1 μM) in combination with ketamine (100 μM) increased cell viability in the MTT assay and reduced the number of apoptotic cells detected by TUNEL and Hoechst 33258 staining. To elucidate a possible mechanism by which 17β-oestradiol exerts its neuroprotective effect, we investigated the PI3K pathway using an inhibitor of PI3K, LY294002. The protective effects of 17β-oestradiol were abrogated by LY294002. Furthermore, we found that 17β-oestradiol not only induced phosphorylation of the PI3K substrate Akt, but also increased the expression of Bcl-2, which down-regulated ketamine-induced caspase-3 activity and inhibited neuronal apoptosis. These data demonstrate that 17β-oestradiol exerts a neuroprotective effect against ketamine-induced neuronal apoptosis by activating the PI3K/Akt/Bcl-2 signalling pathway. Therefore, 17β-oestradiol appears to be a promising agent in preventing or reversing ketamine's toxic effects on neurons at an early developmental stage. © 2013 Nordic Pharmacological Society. Published by John Wiley & Sons Ltd.

Li J.,Hebei General Hospital | Wang B.,Hebei General Hospital | Wu H.,Bethune International Peace Hospital of Chinese PLA | Yu Y.,Bethune International Peace Hospital of Chinese PLA | And 2 more authors.
Brain Research | Year: 2014

Previous studies have demonstrated that the commonly used anesthetic ketamine can induce widespread neuroapoptosis in the neonatal brain and can cause persistent cognitive impairments as the animal matures. Therefore, searching for adjunctive neuroprotective strategies that inhibit ketamine-induced neuroapoptosis and persistent cognitive impairments is highly warranted. The primary goal of this study was to investigate the protective effect of 17β-estradiol against ketamine-induced neuroapoptosis and persistent cognitive impairments in adult rats. Starting from postnatal day 7, Sprague-Dawley male rat pups were given a daily administration of ketamine (75 mg/kg, i.p.) or 17β-estradiol (600 μg/kg, s.c.) in combination with ketamine (75 mg/kg, i.p.). The animals were treated for three consecutive days. 24 h after the last injection, the rats were decapitated, and the prefrontal cortex (PFC) was isolated to detect neuroapoptosis by cleaved caspase-3 immunohistochemistry and by using the TUNEL assay. The neuroactive steroid 17β-estradiol was quantified using high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). The protein levels of BDNF and pAkt were measured by western blot analysis. At two months of age (60 days), the learning and memory abilities were tested using the Morris water maze. The results showed that ketamine triggered significant neuroapoptosis in the neonatal PFC accompanied by the downregulation of 17β-estradiol, BDNF and pAkt. The co-administration of 17β-estradiol with ketamine attenuated these changes. Moreover, 17β-estradiol significantly reversed the learning and memory deficits observed at 60 days of age. In brief, our present data demonstrate that 17β-estradiol attenuates ketamine-induced neuroapoptosis and reverses long-term cognitive deficits in developing rats and thus may be a potential therapeutic and neuroprotective method for the treatment of neurodevelopmental disorders. This article is part of a Special Issue entitled SI: Brain and Memory. © 2014 Elsevier B.V. All rights reserved.

Qin Y.,Hebei Medical University | Chen Z.,Hebei Medical University | Han X.,Bethune International Peace Hospital of Chinese PLA | Wu H.,Bethune International Peace Hospital of Chinese PLA | And 5 more authors.
Journal of Steroid Biochemistry and Molecular Biology | Year: 2015

Progesterone, which acts as a neurosteroid in nervous system, has been shown to have neuroprotective effects in different experiments in vitro and in vivo. Our previous study demonstrates that progesterone exerts neuroprotections in Alzheimer's disease-like rats. Present study attempted to evaluate the protective effects of progesterone on Aβ-treated neurons and potential mechanisms involved in neuroprotection. Results showed that treatment with progesterone protected primary cultured rat cortical neurons against Aβ25-35-induced apoptosis. Furthermore, we observed that progesterone alleviated mitochondrial dysfunction by rescuing mitochondrial membrane potential under Aβ challenge. Moreover, progesterone could also attenuate Bax/Bcl-2 proteins ratio upregulation and inhibit the activation of caspase-3 in Aβ-treated neurons. These indicate that progesterone attenuates Aβ25-35-induced neuronal toxicity by inhibiting mitochondria-associated apoptotic pathway. Both classic progesterone receptors (classic PR) and progesterone receptor membrane component 1 (PGRMC1), a special progesterone membrane receptor, are broadly expressed throughout the brain. The protective effect of progesterone was partially abolished by PGRMC1 inhibitor AG205 rather than classic PR antagonist RU486 in this study. Additionally, progesterone protected neurons by inhibiting Aβ-induced activation of JNK, which was an upstream signaling component in Aβ-induced mitochondria-associated apoptotic pathway. But this process was independent of PGRMC1. Taken together, these results suggest that progesterone exerts a protective effect against Aβ25-35-induced insults at least in part by two complementary pathways: (1) progesterone receptor membrane component 1-dependent inhibition of mitochondrial apoptotic pathway, and (2) blocking Aβ-induced JNK activation. The present study provides new insights into the mechanism by which progesterone brings neuroprotection. This article is part of a Special Issue entitled 'Steroids & Nervous System'. © 2015 Elsevier Ltd. All rights reserved.

PubMed | Capital Medical University and Bethune International Peace Hospital of Chinese PLA
Type: Journal Article | Journal: The international journal of lower extremity wounds | Year: 2015

We aimed to investigate the characteristics of bacterial profiles and antibiotic sensitivity in diabetic foot ulcers before and after wound bed preparation. This study involved 423 diabetic patients with Wagner grades 1 to 4 foot ulcers. Secretion culture was performed before wound bed preparation. The observation endpoint was when the wound showed a tendency toward healing and a specialist determined that stopping antibiotic treatment would not affect wound healing. A second secretion culture was performed after the observation endpoint. We obtained results from both secretion cultures from 411 patients. The proportion of multi-drug-resistant (MDR) gram-positive bacteria was 22.0% and 47.8% before and after treatment, respectively; that for gram-negative bacteria was 3.5% and 19.2%, respectively (P < .05). Pretreatment antibiotic sensitivity of staphylococci and other gram-positive bacteria was 48.7% and 44.8%, respectively; the rates decreased significantly after treatment to 36.8% (P = .031) and 34.8% (P = .027), respectively. Pretreatment antibiotic sensitivity of common and nonfermenting rare gram-negative bacteria was 55.4% and 54.6%, respectively, which decreased substantially after treatment to 33.2% (P = .002) and 32.9% (P = .003), respectively. Wound healing was achieved in 92.7% of patients. Pretreatment and posttreatment C-reactive protein levels were 124.759 71.58 mg/dL and 82.8 53.61 mg/dL, respectively (P < .05). In conclusion, following wound bed preparation for diabetic foot ulcers, MDR bacteria numbers were increased and antibiotic sensitivity was decreased; inflammation was decreased. These findings warrant future studies for confirmation.

PubMed | Bethune International Peace Hospital of Chinese PLA and Hebei Medical University
Type: Journal Article | Journal: Neurological research | Year: 2016

To investigate whether promotion of neuronal differentiation of human umbilical cord mesenchymal stem cells (HUMSCs) by progesterone (PROG) involves changes in brain-derived neurotrophic factor (BDNF) levels.We used rat brain tissue extracts to mimic the brain microenvironment. Quantitative sandwich enzyme-linked immunosorbent assay was performed to measure levels of BDNF in cultured medium with or without PROG.Progesterone increased levels of BDNF in HUMSCs.Progesterone enhancement of brain-derived neurotrophic factor levels may be involved in PROG activated-pathways to promote neuronal differentiation of HUMSCs.

PubMed | Shijiazhuang Hospital of Integrated Traditional Chinese and Western Medicine and Bethune International Peace Hospital of Chinese PLA
Type: Journal Article | Journal: Zhongguo shi yan xue ye xue za zhi | Year: 2015

To explore the molecular mechanism of erythrocyte pyruvate kinase deficiency (PKD).Targeted sequence capture and next-generation sequencing (NGS) were used to detect the regions of exon and exon-intron boundarie of PKLR gene in a clinical suspected PKD patient. The protein function of mutant gene was forecasted by the SIFT and PolyPhen-2 databank, after the mutation of PKLR gene in the patient was detected by the NGS technology, its genotype was confirmed by Sanger sequencing.The patient was found to have peculiar double heterozygous mutations: 661 G>A (Asp221Asn) of exon 5 and 1528 C>T (Arg510Ter) of exon 10, resulting in amino acid substitution Asp221Asn and Arg510Ter, these mutations were also further confirmed by Sanger sequencing. The complex mutations were infrequent and each of them was able to cause diseases.The complex mutations of both 661 G>A and 1528 C>T of PKLR gene are the molecular mechanism of PKD. Simultaneous existance of above-mentioned complex mutations in PDK patient was never been previously reported at home and abroad.

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