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| 1 | Nerve growth factor pretreatment against glutamate-induced hippocampal neuronal injury Action mechanism of phosphatase and tensin homologue deleted on chromosome 10显示文摘BACKGROUND: Nerve growth factor (NGF) attenuates glutamate-induced injury to hippocampal neurons, and the human tumor suppressor gene phosphatase and tensin homologue deleted on chromosome 10 (PTEN) promotes neuronal apoptosis. However, effects of PTEN in NGF-mediated neuroprotection against glutamate excitotoxicity remain poorly understood. OBJECTIVE: To investigate the relationship between NGF inhibition of glutamate-induced injury and PTEN. DESIGN, TIME AND SETTING: The randomized, controlled, in vitro study was performed at the Department of Pathophysiology, Medical School of Nantong University, China from October 2007 to March 2008. MATERIALS: Glutamate, NGF, 4, 6-diamidino-2-phenyl-indolediacetate, 3-[4, 5-dimethylthiazol-2-yl]- 2, 5-diphenyl tetrazoliumbromide (MTT), and lactate dehydrogenase kit (Sigma, USA), fluorescence microscope and inverted phase contrast microscope (Olympus, Japan) were used in this study. METHODS: Hippocampal neurons were obtained from newborn (< 24 hours) Sprague Dawley rats and cultured for 7 days. The control group was not treated with any intervention factor, the glutamate group was treated with glutamate (0.2 mmol/L), and NGF groups were treated with NGF (10, 50, 100, and 200 μg/L, respectively) prior to glutamate treatment. MAIN OUTCOME MEASURES: The MTT and lactate dehydrogenase assays were applied to evaluate viability of hippocampal neurons. Morphological changes in hippocampal neurons were observed using an inverted phase-contrast microscope, and neuronal apoptosis was detected by 4, 6-diamidino-2-phenyl-indolediacetate staining. PTEN mRNA and protein expression were measured by reverse transcription-polymerase chain reaction and Western blot analysis, respectively. RESULTS: Glutamate (0.2 mmol/L) induced significantly decreased neuronal viability and greater lactate dehydrogenase efflux compared with the control group (P < 0.01). However, compared with the glutamate group, cell viability significantly increased and lactate dehydrogenase efflux decreased in the NGF group with increasing NGF concentrations (P < 0.05 or P < 0.01). The apoptotic ratio and PTEN mRNA and protein expression decreased in the NGF group compared with the glutamate group (P < 0.01). CONCLUSION: Pretreatment with NGF exerted neuroprotective effects against glutamate-induced injury, partially through inhibition of PTEN expression and neuronal apoptosis. | Yae Hu Jiahui Mao Yan Zhu Ailing Zhou | 2010 | Neural Regeneration Research2010，5，1： | 12 |
| 2 | Oxymatrine reduces neuroinflammation in rat brain A signaling pathway显示文摘Cerebral neuroinflammation models were established by injecting 10 μg lipopolysaccharide into the hippocampus of male Sprague-Dawley rats. The rats were treated with an intraperitoneal injection of 120, 90, or 60 mg/kg oxymatrine daily for three days prior to the lipopolysaccharide injection. Twenty-four hours after model induction, the hippocampus was analyzed by real-time quantitative PCR, and the cerebral cortex was analyzed by enzyme-linked immunosorbent assay and western blot assay. The results of the enzyme-linked immunosorbent assay and the real-time quantitative PCR showed that the secretion and mRNA expression of the pro-inflammatory cytokines interleukin-1β and tumor necrosis factor-α were significantly decreased in the hippocampus and cerebral cortex of model rats treated with oxymatrine. Western blot assay and real-time quantitative PCR analysis indicated that toll-like receptor 4 mRNA and protein expression were significantly decreased in the groups receiving different doses of oxymatrine. Additionally, 120 and 90 mg/kg oxymatrine were shown to reduce protein levels of nuclear factor-κB p65 in the nucleus and of phosphorylated IκBα in the cytoplasm of brain cells, as detected by western blot assay. Experimental findings indicate that oxymatrine may inhibit neuroinflammation in rat brain via downregulating the expression of molecules in the toll-like receptor 4/nuclear factor-κB signaling pathway. | Jiahui Mao Yae Hu Ailing Zhou Bing Zheng Yi Liu Yueming Du Jia Li Jinyang Lu Pengcheng Zhou | 2012 | Neural Regeneration Research2012，7，30： | 7 |
| 3 | Effect of Nao Yikang on choline acetyltransferase and caspase-3 brain expression in a rat model of Alzheimer's disease显示文摘BACKGROUND: The main components of the traditional Chinese medicine compound Nao Yikanghave been shown to possibly alleviate neural damage.OBJECTIVE: To observe the effects of Nao Yikang on expression of choline acetyltransferase(ChAT) and caspase-3 in the rat brains of an experimental Alzheimer's disease (AD) model, and toinvestigate the mechanisms of potential neuroprotective effects.DESIGN, TIME AND SETTING: A randomized, controlled experiment was performed at theDepartment of Pathophysiology, Medical School of Nantong University between November 2006and December 2007.MATERIALS: The main active components of Nao Yikang were as follows: prepared polygonummultiflorum, Rhizoma anemarrhenae, and Rhizoma acori tatarinowii. Nao Yikang granules wereprepared by Nantong Hospital of Traditional Chinese Medicine. Ibotenic acid (IBO) was purchasedfrom Sigma-Aldrich, USA, ChAT goat anti-rat antibody from Chemicon, USA, and cleaved caspase-3rabbit anti-rat (Asp175) (5A1) antibody from Cell Signaling, USA.METHODS: A total of 60 male, Sprague Dawley rats (2 months old) were randomly assigned to 6groups: sham-surgery, model, Nao Yikang 1.73, 3.45, 6.90 g/kg per day, and piracetam, with 10 ratsin each group. Bilateral infusions of 5 μg IBO into the nucleus basalis of Meynert were performedwith Hamilton syringe and stereotaxic apparatus for AD model establishment. For the sham-surgerygroup, rats received 1 μL saline in the identical stereotaxic position. From the second day, NaoYikang groups were administrated 1.73, 3.45, and 6.90 g/kg per day Nao Yikang, respectively, whilethe piracetam group received 0.04 g/mL piracetam, the model group received 0.5% sodiumcarboxymethyl cellulose, and the sham-surgery group received normal saline. Rats wereintragastrically administered 1 mL/100 g daily for 28 consecutive days.MAIN OUTCOME MEASURES: Following treatment of the various solutions for 28 days, Westernblot was utilized to observe ChAT expression in the frontal cortex of AD rats, andimmunohistochemistry was applied to quantify caspase-3-positive cells in the frontal cortex.RESULTS: ChAT protein expression significantly decreased in the model group (P < 0.01), howevercaspase-3 expression was significantly elevated (P < 0.01) compared with the sham-surgery group.Compared with the model group, ChAT protein expression increased in the Nao Yikang 1.73 g/kgper day, 3.45 g/kg per day, 6.90 g/kg per day groups, and the piracetam group (P < 0.05 or P < 0.01)and the number of caspase-3-positive cells decreased in the Nao Yikang 3.45 g/kg per day and6.90 g/kg per day groups (P < 0.01). However, there was no change in the number ofcaspase-3-positive cells in the 3.45 g/kg per day group.CONCLUSION: The traditional Chinese medicine compound Nao Yikangincreased ChAT proteinexpression and suppressed caspase-3 expression in the frontal cortex in a dose-dependent manner. | Jinsong Geng Hengjian Ni Jiancheng Dong Kui Jiang Ailing Zhou Yae Hu | 2009 | Neural Regeneration Research2009，4，12： | 3 |
| 4 | Role of Toll-like receptor 4 in inflammatory reactions of hippocampal neurons显示文摘Lipopolysaccharide stimulates Toll-like receptor 4 on immune cells to produce immune mediators. Toll-like receptor 4 is also expressed by non-immune cells, which can be stimulated by lipopolysaccharide. However, whether Toll-like receptor 4 is expressed by primary cultured hippocampal neurons and its specific role in lipopolysaccharide-induced neuroinflammation is currently undefined. In this study, Toll-like receptor 4 antibody blocking was used to analyze the Toll-like receptor 4 signaling pathway and changes in inflammation of lipopolysaccharide stimulated hippocampal neurons. Immunofluorescence showed that Toll-like receptor 4 protein was mainly located in the membrane of hippocampal neurons. Quantitative reverse transcription-PCR and western blot assay showed that after stimulation of lipopolysaccharide, the mRNA and protein levels of Toll-like receptor 4 and the mRNA levels of interleukin-1β and tumor necrosis factor-α were significantly increased. In addition, there was increased phosphorylation and degradation of kappa B α inhibitor in the cytosol and increased nuclear factor-κB p65 expression in the nuclei. Pretreatment with Toll-like receptor 4 antibody could almost completely block this increase. These experimental findings indicate that lipopolysaccharide participates in neuroinflammation by stimulating Toll-like receptor 4/nuclear factor-κB pathway in hippocampal neurons, which may be both 'passive victims' and 'activators' of neuroinflammation. | Yae Hu Jiahui Mao Yu Zhang Ailing Zhou | 2013 | Neural Regeneration Research2013，8，16： | 3 |
| 5 | Clinical impact of c-Met expression and its gene amplification in hepatocellular carcinoma显示文摘 | Shunsuke Kondo Hidenori Ojima Hitoshi Tsuda Jun Hashimoto Chigusa Morizane Masafumi Ikeda Hideki Ueno Kenji Tamura Kazuaki Shimada Yae Kanai Takuji Okusaka | 2013 | International Journal of Clinical Oncology2013，，2： | 2 |
| 6 | CD44 Variant Regulates Redox Status in Cancer Cells by Stabilizing the xCT Subunit of System xc ? and Thereby Promotes Tumor Growth显示文摘 | Takatsugu Ishimoto Osamu Nagano Toshifumi Yae Mayumi Tamada Takeshi Motohara Hiroko Oshima Masanobu Oshima Tatsuya Ikeda Rika Asaba Hideki Yagi Takashi Masuko Takatsune Shimizu Tomoki Ishikawa Kazuharu Kai Eri Takahashi Yu Imamura Yoshifumi Baba Mitsuyo O | 2011 | Cancer Cell2011，，3： | 2 |
| 7 | Generation of pluripotent stem cells from adult mouse liver and stomach cells显示文摘 | Aoi T Yae K Nakagawa M | 2008 | Science2008，321，5889： | 1 |
| 8 | Antioxidant activity of theaflavin and thearobigin separaied from Korean mi- crobially fermented tea 显示文摘 | Shon Mi - Yae Park Scok - Kyu Nam Sang - Hae | 2007 | Journal of Food Science and Nutri- tion2007，12，1： | 1 |
| 9 | Influence of cultivar,light condition and pretreatment on adventitious shoot regeneration from leaves,internodes and petioles of Malus domestica Borkh in vitro显示文摘 | Yae Byeongwoo Yang Mihee at al | 1996 | Journal of the Korean Society for Horticultural Science1996，37，5： | 1 |
| 10 | The survival of rat cerebral cortical neurons in the presence of trophic APP peptides 显示文摘 | Yamamoto K Miyoshi T Yae T | 1994 | J Neurobiol1994，25，5： | 1 |
| 11 | Generation of pluripotent stem cells from adult mouse liver and stomach cells显示文摘 | Aoi T Yae K Nakagawa M | 2008 | Science2008，321，5889： | 1 |
| 12 | Generation of pluripotent stem cells from adult mouse liver and stomach cells显示文摘 | Aoi T Yae K Nakagawa M | 2008 | Science2008，321，69： | 1 |
| 13 | Post-ischemic synaptic plasticity in the rat hippocampus after long-term survival:histochemical and autoradiographic study显示文摘 | Onodera H Aoki H Yae T | 1990 | Ncuroscience1990，38，1： | 1 |
| 14 | The formation and growth of bulblets from bulblet sections with swollen basal plate in Lilium oriental hybrid ‘Casa Blanca' 显示文摘 | HAN B H YAE B W GOO D H | 1999 | J Korean Soc Hort Sci1999，40，6： | 1 |
| 15 | Preparation and characterizations of ZnzSiO4:Mn green phosphors 显示文摘 | CHO Yae Hwan CHANG Ho Jtmg | 2003 | Ceram lnt2003，29，： | 1 |
| 16 | Hochuekkito (TJ41), a Kampo formula, ameliorates cachexia induced by colon 26 adenocarcinoma in mice显示文摘 | Yae S Takahashi F Yae T | 2012 | Evid Based Complement Alternat Med2012，2012，97： | 1 |
| 17 | Dopaminergic neuronal loss in transgenic mice expressing the Parkinson’s disease-associated UCH-L1 I93M mutant显示文摘 | Rieko Setsuie Yu-Lai Wang Hideki Mochizuki Hitoshi Osaka Hideki Hayakawa Nobutsune Ichihara Hang Li Akiko Furuta Yae Sano Ying-Jie Sun Jungkee Kwon Tomohiro Kabuta Kenji Yoshimi Shunsuke Aoki Yoshikuni Mizuno Mami Noda Keiji Wada | 2006 | Neurochemistry International2006，，1： | 1 |
| 18 | Mice-lacking LMP2, immuno-proteasome subunit, as an animal model of spontaneous uterine leiomyosarcoma显示文摘Uterine tumors are the most common type of gynecologic neoplasm.Uterine leiomyosarcoma(LMS)is rare,accounting for 2%to 5%of tumors of the uterine body.Uterine LMS develops more often in the muscle tissue layer of the uterine body than in the uterine cervix.The development of gynecologic tumors is often correlated with female hormone secretion;however,the development of uterine LMS is not substantially correlated with hormonal conditions,and the risk factors are not yet known.Radiographic evaluation combined with PET/CT can be useless in the diagnosis and surveillance of uterine LMS.Importantly,a diagnostic biomarker,which distinguishes malignant LMS and benign tumor leiomyoma(LMA)is yet to be established.Accordingly,it is necessary to analyze risk factors associated with uterine LMS in order to establish a method of treatment.LMP2-deficient mice spontaneously develop uterine LMS,with a disease prevalence of~40%by 14 months of age.It is therefore of interest whether human uterine LMS shows a loss of LMP2 expression.We found LMP2 expression is absent in human LMS,but present in human LMA.Therefore,defective LMP2 expression may be one of the risk factors for LMS.LMP2 is potentially a diagnostic biomarker for uterine LMS,and gene therapy with LMP2-encording DNA may be a new therapeutic approach. | Takuma Hayashi Akiko Horiuchi Kenji Sano Nobuyoshi Hiraoka Yae Kanai Tanri Shiozawa Susumu Tonegawa Ikuo Konishi | 2010 | Protein & Cell2010，1，8： | 1 |
| 19 | Development of electrolessly deposited Nano Fe-P films 显示文摘 | Matsuda H Yae S Iwagishi T | 1998 | Trans IMF1998，，76： | 1 |
| 20 | Transport of Nattokinase across the rat intestinal tract显示文摘 | Mitsugu Fujita kyongsu Hong Yae Iro | 1995 | Biol Pharm Bull1995，18，9： | 1 |
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