Publications by authors named "Jiehua Xu"

18 Publications

  • Page 1 of 1

The Microstructure and Reasonable Management of the Arachnoid During the Infrafloccular Approach for Microvascular Decompression of the Facial Nerve.

Turk Neurosurg 2020 Oct 30. Epub 2020 Oct 30.

The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an City, Department of Neurosurgery, Shaanxi Province, The People's Republic of China.

Aim: Arachnoid dissection is a basic step during facial nerve microvascular decompression (MVD). However, the literature focusing on the arachnoid microstructure in this region is scarce, and there are different views on how to handle the arachnoid around the cochlea nerve in order to protect the cochlea nerve. To provide a valuable reference for minimal invasion during facial nerve MVD, the arachnoid microstructure during the infrafloccular approach was studied in this paper.

Material And Methods: This study recruited 55 patients with hemifacial spasm who underwent MVD. Retrospective analyses of the MVD surgical videos were performed to reveal the arachnoid microstructure during the procedures. Cadaveric head specimens (n = 8, on 16 sides) were dissected for observation of the microstructure of the arachnoid in the cerebellopontine angle.

Results: The arachnoid membrane surrounding the facio-cochleovestibular and lower cranial nerves forms two arachnoid sheaths. Both arachnoid sheaths contain two parts: the outer membranous and inner trabecular part. The membranous part is an intact and translucent membrane that wraps around nerves. The inner trabecular part is located beneath the membranous part and forms a trabecular network that connects the membranous arachnoid, nerves, and blood vessels to form a physical structure.

Conclusion: The arachnoid connects the facio-cochleovestibular and lower cranial nerves, blood vessels, and cerebellum as a complex physical entity. Therefore, during MVD surgery, sharply dissecting the arachnoid before retracting the flocculus and relocating the offending vessels helps reduce nerve injury.
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http://dx.doi.org/10.5137/1019-5149.JTN.31625-20.2DOI Listing
October 2020

Author Correction: RhMYB108, an R2R3-MYB transcription factor, is involved in ethylene- and JA-induced petal senescence in rose plants.

Hortic Res 2019 Dec 27;6(1):139. Epub 2019 Dec 27.

School of Applied Chemistry and Biological Technology, Postdoctoral Innovation Practice Base, Shenzhen Polytechnic, Shenzhen, Guangdong, 518055, China.

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http://dx.doi.org/10.1038/s41438-019-0230-7DOI Listing
December 2019

First report of powdery mildew of crape jasmine () caused by in China.

Plant Dis 2020 Oct 13. Epub 2020 Oct 13.

Shenzhen Polytechnic, 47891, Shenzhen, Guangdong, China;

Crape jasmine (Tabernaemontana divaricata) is a popular flowering shrub widely grown in southern China. Its leaves and roots are used in Chinese traditional medicine. In December, 2019, powdery mildew symptoms were observed on five crape jasmine shrubs on the campus of Shenzhen Polytechnic (22°35'N; 113°56'E), in Guangdong province. Approximately 45% of leaves were infected. Symptoms initially appeared as circular to irregular white patches on the leaf petiole, and subsequently coalesced to develop into abundant hyphal growth on both sides of the leaves, which soon wilted. Hyphae were septate, branched, with simple kidney-shaped to moderately lobed appressoria. Conidia formed singly, ellipsoid-ovoid to subcylindrical, 27-37 × 14-20 μm (mean 32±2.5 × 17±1.6 μm), with a length/width ratio varying from 1.3 to 2.4. Conidiophores were erect, unbranched, consisted of two cells, 60 to 84 μm long (mean 73±4 μm), and with straight to severely kinked cylindrical foot-cells at the base, 29-35 × 3-7 μm (mean 32±3 × 6±2 μm). Chasmothecia were not observed on sampled plants. These morphological characteristics were typical to the conidial stage of the genus Erysiphe (Braun and Cook, 2012). For molecular identification, genomic DNA was extracted from conidia washed from infected leaves and using Fungal DNA Kit (Omega Bio-tek Inc., Guangzhou, China). Semi-nested PCR amplification of the internal transcribed spacer (ITS) region of rDNA was conducted by using primer sets P3 (Kusaba et al., 1995)/ITS5 and ITS5/ITS4 (White et al., 1990) for the first and second reactions, respectively. BLASTn analysis of the obtained 719 bp sequence (GenBank Accession No. MT802112) showed 99.7% identity with those of E. elevata (KY660910, MH985631, MK253282). On the basis of morphological and molecular analyses, the fungus was identified as Erysiphe elevata. To confirm pathogenicity, infected leaves were gently pressed onto healthy leaves of three healthy plants in separate pots, and three noninoculated plants were used as controls. All plants were maintained in a greenhouse at 25 ℃, and relative humidity of 50 to 65%. After 11 days, similar disease symptoms were observed on the inoculated plants while no symptoms developed on control plants. The fungus observed on the inoculated shrubs was identical morphologically to that o the original infected leaves. E. elevata is a common powdery mildew species infecting Catalpa spp. (Cook et al., 2006), Plumeria rubra (Wu et al., 2019; Yeh et al., 2019) and Eucalyptus camaldulensis (Meeboon and Takamatsu, 2017). However, no powdery mildew were found on P. rubra nearby. To our knowledge, this is the first report of this fungus infecting T. divaricata.
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http://dx.doi.org/10.1094/PDIS-08-20-1717-PDNDOI Listing
October 2020

Erratum: Author Correction: RhMYB108, an R2R3-MYB transcription factor, is involved in ethylene- and JA-induced petal senescence in rose plants.

Hortic Res 2019;6:139. Epub 2019 Dec 27.

1School of Applied Chemistry and Biological Technology, Postdoctoral Innovation Practice Base, Shenzhen Polytechnic, Shenzhen, Guangdong 518055 China.

[This corrects the article DOI: 10.1038/s41438-019-0221-8.].
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http://dx.doi.org/10.1038/s41438-019-0230-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6932989PMC
December 2019

LncMSEN1, a mantle-specific LncRNA participating in nacre formation and response to polyI:C stimulation in pearl oyster Pinctada fucata martensii.

Fish Shellfish Immunol 2020 Jan 10;96:330-335. Epub 2019 Dec 10.

Fishery College, Guangdong Ocean University, Zhanjiang, 524025, China. Electronic address:

Long noncoding RNA (LncRNA) regulates various life processes, including biomineralization and innate immune response through complex mechanisms. In this research, we identified a LncRNA named LncMSEN1 from pearl oyster Pinctada fucata martensii. LncMSEN1 sequence was validated by PCR, and its expression was high in mantle tissues according to qRT-PCR. LncMSEN1 was co-located with the nacre matrix protein N-U8 and fibrinogen domain-containing protein. And LncMSEN1 and N-U8 expression levels in the mantle were positively correlated. RNA interference was used to detect its effect on nacre formation in shells. Results showed that the decreased LncMSEN1 expression in mantle can cause the disordered growth of crystals on the inner surface of nacre in the shells, as well as the decrease expression of N-U8. In addition, the LncMSEN1 expression level significantly increased at 24 h after polyI:C stimulation in the mantle (P < 0.05). These findings suggested the involvement of LncMSEN1 in the formation of nacre in shells and related to innate immune response in pearl oyster, which provided additional insights into the roles of LncRNAs in pearl oysters.
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http://dx.doi.org/10.1016/j.fsi.2019.12.015DOI Listing
January 2020

RhMYB108, an R2R3-MYB transcription factor, is involved in ethylene- and JA-induced petal senescence in rose plants.

Hortic Res 2019 1;6:131. Epub 2019 Dec 1.

1School of Applied Chemistry and Biological Technology, Postdoctoral Innovation Practice Base, Shenzhen Polytechnic, Shenzhen, Guangdong 518055 China.

Rose () plants are major ornamental species worldwide, and their commercial value greatly depends on their open flowers, as both the quality of fully open petals and long vase life are important. Petal senescence can be started and accelerated by various hormone signals, and ethylene is considered an accelerator of petal senescence in rose. To date, however, the underlying mechanism of signaling crosstalk between ethylene and other hormones such as JA in petal senescence remains largely unknown. Here, we isolated , an R2R3-MYB transcription factor, which is highly expressed in senescing petals as well as in petals treated with exogenous ethylene and JA. Applications of exogenous ethylene and JA markedly accelerated petal senescence, while the process was delayed in response to applications of 1-MCP, an ethylene action inhibitor. In addition, silencing of alter the expression of SAGs such as , , , , and , and finally block ethylene- and JA-induced petal senescence. Furthermore, RhMYB108 was identified to target the promoters of , , and . Our results reveal a model in which functions as a receptor of ethylene and JA signals to modulate the onset of petal senescence by targeting and enhancing senescence-associated gene expression.
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http://dx.doi.org/10.1038/s41438-019-0221-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6885062PMC
December 2019

Progranulin protects against cerebral ischemia-reperfusion (I/R) injury by inhibiting necroptosis and oxidative stress.

Biochem Biophys Res Commun 2020 01 31;521(3):569-576. Epub 2019 Oct 31.

Department of Anesthesiology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, Shaanxi, China. Electronic address:

Ischemic stroke is a leading cause of mortality and disability worldwide. Nevertheless, its molecular mechanisms have not yet been adequately illustrated. Progranulin (PGRN) is a secreted glycoprotein with pleiotropic functions. In the present study, we found that PGRN expression was markedly reduced in mice after stroke onset through middle cerebral artery occlusion (MCAO). We also showed that necroptosis was a mechanism underlying cerebral I/R injury. Importantly, PGRN knockdown in vivo significantly promoted the infarction volume and neurological deficits scores in mice after MCAO surgery. Necroptosis induced by MCAO was further accelerated by PGRN knockdown, as evidenced by the promoted expression of phosphorylated receptor-interacting protein (RIP) 1 kinase (RIPK1), RIPK3 and mixed lineage kinase domain-like (MLKL), which was accompanied with increased expression of cleaved Caspase-8 and Caspase-3. However, PGRN over-expression was neuroprotective. Additionally, PGRN-regulated ischemic stroke was related to ROS accumulation that MCAO-mice with PGRN knockdown exhibited severe oxidative stress, as proved by the aggravated malondialdehyde (MDA) and lipid peroxidation (LPO) contents, and the decreased superoxide dismutase (SOD) activity. However, PGRN over-expression in mice with cerebral ischemia showed anti-oxidative effects. Finally, PGRN was found to attenuate oxidative damage partly via its regulatory effects on necroptosis. Therefore, promoting PGRN expression could reduced cerebral I/R-induced brain injury by suppressing neroptosis and associated reactive oxygen species (ROS) production. These data elucidated that PGRN might provide an effective therapeutic treatment for ischemic stroke.
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http://dx.doi.org/10.1016/j.bbrc.2019.09.111DOI Listing
January 2020

Whole Exome Sequencing Identified a Novel Heterozygous Mutation in Gene in a Chinese Patient With Acute Intermittent Porphyria With Rare Type of Mild Anemia.

Front Genet 2018 20;9:129. Epub 2018 Apr 20.

Department of Cell Biology and Medical Genetics, School of Medicine, Zhejiang University, Hangzhou, China.

Acute intermittent porphyria (AIP) is a rare hereditary metabolic disease with an autosomal dominant mode of inheritance. Germline mutations of gene causes AIP. Mutation of gene results into the partial deficiency of the heme biosynthetic enzyme hydroxymethylbilane synthase. AIP is clinically manifested with abdominal pain, vomiting, and neurological complaints. Additionally, an extreme phenotypic heterogeneity has been reported in AIP patients with mutations in gene. Here, we investigated a Chinese patient with AIP. The proband is a 28-year-old Chinese male manifested with severe stomach ache, constipation, nausea and depression. Proband's father and mother is normal. Proband's blood sample was collected and genomic DNA was extracted. Whole exome sequencing and Sanger sequencing identified a heterozygous novel single nucleotide deletion (c.809delC) in exon 12 of gene in the proband. This mutation leads to frameshift followed by formation of a truncated (p.Ala270Valfs2) HMBS protein with 272 amino acids comparing with the wild type HMBS protein of 361 amino acids. This mutation has not been found in proband's unaffected parents as well as in 100 healthy normal control. According to the variant interpretation guidelines of American College of Medical Genetics and Genomics (ACMG), this variant is classified as variant. Our findings expand the mutational spectra of gene related AIP which are significant for screening and genetic diagnosis for AIP.
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http://dx.doi.org/10.3389/fgene.2018.00129DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5920022PMC
April 2018

Necrostatin-1 protects C2C12 myotubes from CoCl2-induced hypoxia.

Int J Mol Med 2018 May 6;41(5):2565-2572. Epub 2018 Feb 6.

Guangdong Traditional Medical and Sports Injury Rehabilitation Research Institute, Guangdong Second Provincial General Hospital, Guangzhou, Guangdong 510317, P.R. China.

Necrostatin-1 (Nec-1) is a selective and potent allosteric inhibitor of necroptosis by specifically inhibiting the activity of receptor‑interacting protein (RIP) 1 kinase. The aim of the present study was to determine the effect of Nec‑1 on an anoxia model comprising mouse skeletal C2C12 myotubes. In the present study, a hypoxic mimetic reagent, cobalt chloride (CoCl2), was used to induce hypoxia in C2C12 myotubes. The cytotoxic effects of CoCl2‑induced hypoxia were determined by a Cell Counting kit‑8 assay and flow cytometry. Transmission electron microscopy (TEM) was used to characterize the morphological characteristics of dead cells at the ultrastructural level. To clarify the signaling pathways in CoCl2‑mediated cell death, the expression levels of RIP1, RIP3, extracellular signal‑regulated kinase (ERK)1/2, hypoxia‑inducible factor (HIF)‑1α and B cell lymphoma‑2 adenovirus E1B 19‑kDa interacting protein 3 (BNIP3) were investigated by western blotting. Oxidative stress was determined using 2',7'‑dichlorofluorescin diacetate to measure intracellular reactive oxygen species (ROS) and the fluorescent dye JC‑1 was used to measure mitochondrial membrane potential (Δψm). The results showed that the ratios of apoptotic and necrotic C2C12 cells were increased following CoCl2 treatment, typical necroptotic morphological characteristics were able to observe by TEM, whereas Nec‑1 exhibited a protective effect against CoCl2‑induced oxidative stress. Treatment with Nec‑1 significantly decreased the levels of RIP1, p‑ERK1/2, HIF‑1α, BNIP3 and ROS induced by CoCl2, and promoted C2C12 differentiation. Nec‑1 reversed the CoCl2‑induced decrease in mitochondrial membrane potential. Together, these findings suggested that Nec‑1 protected C2C12 myotubes under conditions of CoCl2-induced hypoxia.
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http://dx.doi.org/10.3892/ijmm.2018.3466DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5846651PMC
May 2018

Effects of Cobalt Chloride, a Hypoxia-Mimetic Agent, on Autophagy and Atrophy in Skeletal C2C12 Myotubes.

Biomed Res Int 2017 19;2017:7097580. Epub 2017 Jun 19.

Department of Hematology, Guangdong No. 2 Provincial People's Hospital, 466 Xin Gang Zhong Road, Guangzhou 510317, China.

Background: Hypoxia-induced autophagy and muscle wasting occur in several environmental and pathological conditions. However, the molecular mechanisms underlying the effects of the hypoxia-mimetic agent CoCl on autophagy and muscle atrophy are still unclear.

Methods: C2C12 myotubes were exposed to increasing concentrations of CoCl for 24 hours. Quantitative RT-PCR, Western blotting, and transmission electron microscopy were performed to confirm autophagy occurs. Autophagy proteins were measured to understand the molecule mechanisms. We also inhibited hypoxic autophagy and examined the changes in myogenin expression, myotubes formation, and apoptosis.

Results: Our results showed that CoCl-mimicked hypoxia upregulated the expression of the autophagy-related proteins LC3, HIF-1, BNIP3, p-AMPK, and beclin-1, whereas p62 and p-mTOR were downregulated. In addition, the autophagosome could be observed after CoCl induction. The expression of the autophagy-related E3 ligase parkin and the muscle-specific ubiquitin ligase atrogin-1 was increased by CoCl. Inhibition of autophagy by 3MA increased myogenin expression and promoted myotubes formation and the percentage of cell death was decreased.

Conclusions: Our results confirmed that CoCl-mimicked hypoxia induced autophagy via the HIF-1/BNIP3/beclin-1 and AMPK/mTOR pathways. Our results also revealed an important link between autophagy and muscle atrophy under hypoxia, which may help to develop new therapeutic strategies for muscle diseases.
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http://dx.doi.org/10.1155/2017/7097580DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5494548PMC
April 2018

Lower Bone Mineral Density in Patients with Parkinson's Disease: A Cross-Sectional Study from Chinese Mainland.

Front Aging Neurosci 2015 27;7:203. Epub 2015 Oct 27.

Department of Neurology, The Third Affiliated Hospital of Sun Yat-Sen University , Guangzhou , China.

Key Points: Significantly lower BMD in PD compared to healthy subjects in both genders.Less than 35 mg(2)/dl(2) of Ca-P product in >80% of PD patients.Significant correlations between BMD and severity of PD.Lower BMD at H&Y stage III/IV than that at H&Y stage I/II.

Objectives: Although several lines of evidence have suggested that patients with Parkinson's disease (PD) have a higher risk of osteoporosis and fracture, the association between bone mineral density (BMD) and severity of PD patients is unknown.

Methods: We performed a cross-sectional study of 54 patients with PD and 59 healthy age-matched controls. Multiple clinical scales were used to evaluate the severity of PD, and serum levels of calcium, phosphorus, and homocysteine were measured to determine BMD's association with PD severity.

Results: BMD in PD patients was significantly lower than that in healthy controls. The BMD scores of the spine, femoral neck (FN), and hip were lower in females than in males in the healthy group. In the PD group, BMD in the hip was significantly lower in females compared to males. There was a negative correlation between daily l-DOPA dosage and BMD in the spine and hip in the PD group, while BMD in the spine, neck, and hip was significantly correlated with severity of PD. Besides, we found that among the lumbar spine (LS), FN, and hip, bone loss in the LS was the most severe in PD patients based on the T-scores.

Conclusion: Our findings support the hypothesis that patients with PD have a higher risk of osteoporosis, and that low BMD in the spine, FN, and hip may indirectly reflect the severity of PD. Our findings have prompted us to pay more attention to osteoporosis in the LS in Chinese PD patients.
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http://dx.doi.org/10.3389/fnagi.2015.00203DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4621433PMC
November 2015

Molecular Recognition of Human Liver Cancer Cells Using DNA Aptamers Generated via Cell-SELEX.

PLoS One 2015 4;10(5):e0125863. Epub 2015 May 4.

Department of Chemistry, Department of Biochemistry and Molecular Biology and Department of Physiology and Functional Genomics, Center for Research at the Bio/Nano Interface, Health Cancer Center, UF Genetics Institute and McKnight Brain Institute, University of Florida, Gainesville, FL, United States of America.

Most clinical cases of liver cancer cannot be diagnosed until they have evolved to an advanced stage, thus resulting in high mortality. It is well recognized that the implementation of early detection methods and the development of targeted therapies for liver cancer are essential to reducing the high mortality rates associated with this disease. To achieve these goals, molecular probes capable of recognizing liver cancer cell-specific targets are needed. Here we describe a panel of aptamers able to distinguish hepatocarcinoma from normal liver cells. The aptamers, which were selected by cell-based SELEX (Systematic Evolution of Ligands by Exponential Enrichment), have Kd values in the range of 64-349 nM toward the target human hepatoma cell HepG2, and also recognize ovarian cancer cells and lung adenocarcinoma. The proteinase treatment experiment indicated that all aptamers could recognize target HepG2 cells through surface proteins. This outcome suggested that these aptamers could be used as potential probes for further research in cancer studies, such as developing early detection assays, targeted therapies, and imaging agents, as well as for the investigation of common membrane proteins in these distinguishable cancers.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0125863PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4418664PMC
February 2016

A survey of advancements in nucleic acid-based logic gates and computing for applications in biotechnology and biomedicine.

Chem Commun (Camb) 2015 Mar;51(18):3723-34

Center for Research at Bio/Nano Interface, Department of Chemistry and Department of Physiology and Functional Genomics, Shands Cancer Center, UF Genetics Institute and McKnight Brain Institute, University of Florida, Gainesville, Florida 32611-7200, USA.

Nucleic acid-based logic devices were first introduced in 1994. Since then, science has seen the emergence of new logic systems for mimicking mathematical functions, diagnosing disease and even imitating biological systems. The unique features of nucleic acids, such as facile and high-throughput synthesis, Watson-Crick complementary base pairing, and predictable structures, together with the aid of programming design, have led to the widespread applications of nucleic acids (NA) for logic gate and computing in biotechnology and biomedicine. In this feature article, the development of in vitro NA logic systems will be discussed, as well as the expansion of such systems using various input molecules for potential cellular, or even in vivo, applications.
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http://dx.doi.org/10.1039/c4cc10047fDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4442017PMC
March 2015

Self-assembly of DNA nanohydrogels with controllable size and stimuli-responsive property for targeted gene regulation therapy.

J Am Chem Soc 2015 Feb 26;137(4):1412-5. Epub 2015 Jan 26.

The Key Lab of Analysis and Detection Technology for Food Safety of the MOE, Fujian Provincial Key Laboratory of Analysis and Detection Technology for Food Safety, College of Chemistry, Fuzhou University , Fuzhou 350002, P.R. China.

Here, we report the synthesis and characterization of size-controllable and stimuli-responsive DNA nanohydrogels as effective targeted gene delivery vectors. DNA nanohydrogels were created through a self-assembly process using three kinds of building units, respectively termed Y-shaped monomer A with three sticky ends (YMA), Y-shaped monomer B with one sticky end (YMB), and DNA linker (LK) with two sticky ends. Hybridization at the sticky ends of monomers and LK leads to nanohydrogel formation. DNA nanohydrogels are size-controllable by varying the ratio of YMA to YMB. By incorporating different functional elements, such as aptamers, disulfide linkages, and therapeutic genes into different building units, the synthesized aptamer-based nanohydrogels (Y-gel-Apt) can be used for targeted and stimuli-responsive gene therapy. Y-gel-Apt strongly inhibited cell proliferation and migration in target A549 cells, but not in control cells. By taking advantage of facile modular design and assembly, efficient cellular uptake, and superior biocompatibility, this Y-gel-Apt holds great promise as a candidate for targeted gene or drug delivery and cancer therapy.
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http://dx.doi.org/10.1021/ja512293fDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4449038PMC
February 2015

Protective effects of astragaloside IV against amyloid beta1-42 neurotoxicity by inhibiting the mitochondrial permeability transition pore opening.

PLoS One 2014 6;9(6):e98866. Epub 2014 Jun 6.

Department of Human Anatomy and Histo-Embryology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China.

Mitochondrial dysfunction caused by amyloid β-peptide (Aβ) plays an important role in the pathogenesis of Alzheimer disease (AD). Substantial evidence has indicated that the mitochondrial permeability transition pore (mPTP) opening is involved in Aβ-induced neuronal death and reactive oxygen species (ROS) generation. Astragaloside IV (AS-IV), one of the major active constituents of Astragalus membranaceus, has been reported as an effective anti-oxidant for treating neurodegenerative diseases. However, the molecular mechanisms still need to be clarified. In this study, we investigated whether AS-IV could prevent Aβ1-42-induced neurotoxicity in SK-N-SH cells via inhibiting the mPTP opening. The results showed that pretreatment of AS-IV significantly increased the viability of neuronal cells, reduced apoptosis, decreased the generation of intracellular reactive oxygen species (ROS) and decreased mitochondrial superoxide in the presence of Aβ1-42. In addition, pretreatment of AS-IV inhibited the mPTP opening, rescued mitochondrial membrane potential (ΔΨm), enhanced ATP generation, improved the activity of cytochrome c oxidase and blocked cytochrome c release from mitochondria in Aβ1-42 rich milieu. Moreover, pretreatment of AS-IV reduced the expression of Bax and cleaved caspase-3 and increased the expression of Bcl-2 in an Aβ1-42 rich environment. These data indicate that AS-IV prevents Aβ1-42-induced SK-N-SH cell apoptosis via inhibiting the mPTP opening and ROS generation. These results provide novel insights of AS-IV for the prevention and treatment of neurodegenerative disorders such as AD.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0098866PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4048237PMC
January 2015

Activation of SIRT1 by curcumin blocks the neurotoxicity of amyloid-β25-35 in rat cortical neurons.

Biochem Biophys Res Commun 2014 May 19;448(1):89-94. Epub 2014 Apr 19.

Department of Human Anatomy and Histo-Embryology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi 710061, China. Electronic address:

As one of the most important hallmarks of Alzheimer's disease (AD), β-amyloid (Aβ) plays important roles in inducing reactive oxygen species (ROS) generation, mitochondrial dysfunction and apoptotic cell death in neurons. Curcumin extracted from the yellow pigments spice plant turmeric shows multiplied bioactivities such as antioxidant and anti-apoptosis properties in vitro and in vivo. In the present study, the neuroprotective effect of curcumin against Aβ25-35-induced cell death in cultured cortical neurons was investigated. We found that pretreatment of curcumin prevented the cultured cortical neurons from Aβ25-35-induced cell toxicity. In addition, curcumin improved mitochondrial membrane potential (ΔΨm), decreased ROS generation and inhibited apoptotic cell death in Aβ25-35 treated neurons. Furthermore, we found that application of curcumin activated the expression of SIRT1 and subsequently decreased the expression of Bax in the presence of Aβ25-35. The protective effect of curcumin was blocked by SIRT1 siRNA. Taken together, our results suggest that activation of SIRT1 is involved in the neuroprotective action of curcumin.
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http://dx.doi.org/10.1016/j.bbrc.2014.04.066DOI Listing
May 2014

Multiple metastases in a novel LNCaP model of human prostate cancer.

Oncol Rep 2013 Aug 26;30(2):615-22. Epub 2013 Feb 26.

Department of Nuclear Medicine, the Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong 510630, PR China.

Metastasis is a frequent and lethal consequence of prostate cancer. Current treatments for metastasis are palliative only. Thus, experimental animal models of metastatic prostate cancer are required for investigations of its pathogenesis and for the development of treatment strategies; however, few models exist at present. In the present study, the LNCaP prostate cancer cell line was co-transfected with a PGK-luciferase-GFP lentivirual vector (LNCaP-luc). Repeated subcutaneous injections of LNCaP-luc cells with Matrigel in nude mice followed by isolation of the cells from tumors resulted in the generation of the LNCaP1-luc cell line. We used CCK-8 and Transwell migration assays, western blot analysis and polymerase chain reaction to detect differences in the characteristics between the LNCaP-luc and LNCaP1-luc cells, and used LNCaP cells to generate a mouse model of metastatic prostate cancer by intracardiac injection. Metastasis was evaluated by bioluminescence imaging, and histological and immunohistochemical staining. the characteristics of the LNCaP1-luc cells differed from those of LNCaP cells, and LNCaP1-luc cells showed increased cell proliferation, cell invasion, tumorigenicity and metastasis potential, and underwent epithelial-mesenchymal transition. In addition, the LNCaP1-luc cells induced multiple metastases in mice when injected into the left cardiac muscle.
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http://dx.doi.org/10.3892/or.2013.2305DOI Listing
August 2013

Biomechanical study of anterior cervical corpectomy and step-cut grafting with bioabsorbable screws fixation in cadaveric cervical spine model.

Spine (Phila Pa 1976) 2006 Sep;31(19):2195-201

Department of Orthopaedic Surgery, the 2nd Hospital of Xi'an Jiaotong University, PR China.

Study Design: An in vitro biomechanical study.

Objective: To determine the initial stability of a novel construct in a 1-level cadaveric cervical spine model by comparing it with a conventional method.

Summary Of Background Data: Lots of endeavors have been made to enhance fusion rates and reduce complications in the anterior cervical spine procedure.

Methods: There were 12 fresh human cadaveric cervical spines (C3-C7) randomly divided into 2 groups: group 1, 1-level corpectomy of C5 and step-cut grafting with bioabsorbable screw fixation (SCAS); and group 2, 1-level corpectomy of C5 and strut grafting with anterior plate fixation (SP). For each specimen, the intact underwent a flexibility test first, followed by the instrumented construct. Rotational angles of the C4-C6 segment were measured to study the immediate stability of anterior cervical corpectomy and SCAS, compared with the intact and anterior cervical corpectomy and SP.

Results: Both anterior cervical corpectomy with SCAS and with SP significantly (P < 0.01) decreased the motions of C4-C6 in all 6 degrees of freedom after instrumentation. Compared with anterior cervical corpectomy and SP, anterior cervical corpectomy and SCAS had higher stability (P < 0.05) in extension, and comparable stability (P > 0.05) in flexion and axial rotation, but lower stability (P
Conclusion: Anterior cervical corpectomy and SCAS, a novel method of anterior cervical spine decompression and reconstruction, was introduced. The in vitro biomechanical study showed that anterior cervical corpectomy and SCAS had sufficient immediate stability except for the lateral bending, compared with anterior cervical corpectomy and SP, in a 1-level cadaveric cervical spine model. However, an animal experimental in vivo evaluation of anterior cervical corpectomy and SCAS still has to be performed.
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http://dx.doi.org/10.1097/01.brs.0000232798.97075.73DOI Listing
September 2006