http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Dengue Virus 2 NS2B Targets MAVS and IKKε to Evade the Antiviral Innate Immune Response
Nie Ying,Deng Dongqing,Mou Lumin,Long Qizhou,Chen Jinzhi,Wu Jiahong 한국미생물·생명공학회 2023 Journal of microbiology and biotechnology Vol.33 No.5
Dengue virus (DENV) is a widespread arbovirus. To efficiently establish infection, DENV evolves multiple strategies to hijack the host innate immune response. Herein, we examined the inhibitory effects of DENV serotype 2 (DENV2) nonstructural proteins on RIG-I-directed antiviral immune response. We found that DENV2 NS2A, NS2B, NS4A, and NS4B significantly inhibited RIG-I-mediated IFN-β promoter activation. The roles of NS2B in RIG-I-directed antiviral immune response are unknown. Our study further showed that NS2B could dose-dependently suppress RIG-I/MAVSinduced activation of IFN-β promoter. Consistently, NS2B significantly decreased RIG-I- and MAVSinduced transcription of IFNB1, ISG15, and ISG56. Mechanistically, NS2B was found to interact with MAVS and IKKε to impair RIG-I-directed antiviral response. Our findings demonstrated a previously uncharacterized function of NS2B in RIG-I-mediated antiviral response, making it a promising drug target for anti-DENV treatments.
Ying-Jie Niu,Kyung-Tae Shin,Wenjun Zhou,Zheng-Wen Nie,Junchul David Yoon,Nam-Hyung Kim,Xiang-Shun Cui 한국동물생명공학회(구 한국동물번식학회) 2017 발생공학 국제심포지엄 및 학술대회 Vol.2017 No.10
C-phycocyanin (C-PC) is a biliprotein enriched in blue-green algae that is known to possess antioxidant, antiapoptosis, anti-inflammatory, and radical-scavenging properties in somatic cells. But the protective effect of C-PC on porcine embryo developmental competence in in vitro is little known. In the present study, we investigated the effect of C-PC on the development of porcine early embryos as well as the underlying its mechanisms. Different concentrations of C-CP (1, 2, 5, 8, 10 μg/mL) was added to the porcine zygote medium 5 (PZM-5) during in vitro culture. The results showed that 5 μg/mL C-PC significantly increased blastocyst formation. Blastocyst formation and its quality were significantly increased in 50 μM H2O2 treatment group following 5μg/mL C-PC addition. C-PC prevented H2O2-induced compromise of mitochondrial membrane potential, release of cytochrome C from the mitochondria and reactive oxygen species generation. Furthermore, apoptosis, DNA damage level and autophagy in the blastocysts were attenuated by supplement of C-PC in H2O2-induce doxidativ injury group compared with control.Taken together, these results suggest that C-PC has beneficial effects on the development of porcine parthenotes by attenuating mitochondrial dysfunction and oxidative stress.
Ying-Jie Niu,Dongjie Zhou,Wenjun Zhou,Zheng-Wen Nie,Ju-Yeon Kim,YoungJin Oh,So-Rim Lee,Xiang-Shun Cui 한국동물생명공학회(구 한국동물번식학회) 2020 Journal of Animal Reproduction and Biotechnology Vol.35 No.1
Nitric oxide (NO)-induced protein S-nitrosylation triggers mitochondrial dysfunction and was related to cell senescence. However, the exact mechanism of these damages is not clear. In the present study, to investigate the relationship between in vitro aging and NO-induced protein S-nitrosylation, oocytes were treated with sodium nitroprusside dihydrate (SNP), and the resultant S-nitrosylated proteins were detected through biotin-switch assay. The results showed that levels of protein S-nitroso thiols (SNO)s and expression of S-nitrosoglutathione reductase (GSNOR) increased, while activity and function of mitochondria were impaired during oocyte aging. Addition of SNP, a NO donor, to the oocyte culture led to accelerated oocyte aging, increased mitochondrial dysfunction and damage, apoptosis, ATP deficiency, and enhanced ROS production. These results suggested that the increased NO signal during oocyte aging in vitro, accelerated oocyte degradation due to increased protein S-nitrosylation, and ROS-related redox signaling.
Ying Yang,Wei Nie,Jianmin Yuan,Bingkun Zhang,Zhong Wang,Zhenlong Wu,Yuming Guo 생화학분자생물학회 2010 Experimental and molecular medicine Vol.42 No.11
Deregulation of endothelial nitric oxide synthase (eNOS)plays an important role in the development of multiple cardiovascular diseases. Our recent study demonstrated that genistein supplementation attenuates pulmonary arterial hypertension in broilers by restoration of endothelial function. In this study, we investigated the molecular mechanism by using broiler pulmonary arterial endothelial cells (PAECs). Our results showed that genistein stimulated a rapid phosphorylation of eNOS at Ser1179 which was associated with activation of eNOS/NO axis. Further study indicated that the activation of eNOS was not mediated through estrogen receptors or tyrosine kinase inhibition, but via a phosphatidylinositol 3-kinase (PI3K)/Akt-dependent signaling pathway, as the eNOS activity and related NO release were largely abolished by pharmacological inhibitors of PI3K or Akt. Thus, our findings revealed a critical function of Akt in mediating genistein-stimulated eNOS activity in PAECs, partially accounting for the beneficial effects of genistein on the development of cardiovascular diseases observed in animal models.
Nie Chun yan,He Fang,Xia Ying,Wang Ju 보안공학연구지원센터 2016 International Journal of u- and e- Service, Scienc Vol.9 No.12
Physiological information can objectively reflect the emotional state. Emotion recognition based on physiological signals has the important practical application value. In this paper, six kinds of chaotic characteristics were extracted from physiological data about Electromyogram, Skin conductivity, Respiration, which come from Augsburg university in Germany. Six kinds of chaotic characteristics contain the largest Lyapunov exponent, correlation dimension, box dimensions, information entropy, approximate entropy and complexity. On the basis of this, the degree of relation between chaotic characteristics of physiological signals and emotions was researched. The results showed that different chaotic characteristic values of different physiological signals sensitive to the emotion is different. Therefore, in order to improve the recognition rate, the chaotic characteristics of the multiple physiological information need to be merged to establish chaos matrix, which provide a new method for emotion recognition.
Melatonin enhances mitochondrial biogenesis and function in porcine preimplantation embryos
Ying-Jie Niu,Wenjun Zhou,Zheng-Wen Nie,Kyung-Tae Shin,Yong-Han Kim,Xiang-Shun Cui 한국수정란이식학회 2018 한국수정란이식학회 학술대회 Vol.2018 No.11
Melatonin (N-aceyl-5-methoxytryptamine) is the major hormone of the pineal gland. Melatonin and its metabolic derivatives possess extensive free-radical scavenging abilities and played critical roles in antioxidative stress, resisting apoptotic cell death. Melatonin also could enhance mitochondrial biogenesis in rats with carbon tetrachloride-induced liver fibrosis. In addition, melatonin attenuates myocardial ischemia/reperfusion injury by reducing oxidative stress damage via activation of SIRT1 signaling in a melatonin receptor 2-dependent manner. Activation or overexpression of SIRT1 could enhance mitochondrial biogenesis and function by inducing PGC-1α expression and deacetylation. The aim of this study was to investigate if melatonin enhances mitochondrial biogenesis and function via activation of melatonin receptor 2/SIRT1/PGC1-α Pathway. The results showed that Melatonin rescued rotenone-induced impairment of porcine embryo development. Treatment with rotenone could increase oxidative stress and apoptosis. Rotenone impaired mitochondrial functions by disrupting mitochondrial membrane potential, reducing mitochondrial DNA copy number and ATP production. Melatonin could improve SIRT1 and PGC-1α expression, inducing mitochondrial biogenesis. Rotenone-induced mitochondrial dysfunction and ATP deficiency was rescued by melatonin treatment, the oxidative stress and apoptosis was significantly decreased. Inhibition of melatonin receptor 2 or Knockdown of SIRT1 abolished the protective effects of melatonin on rotenone-induced impairments. Therefore, melatonin enhanced mitochondrial biogenesis and function, protected against rotenone-induced impairments.
Niu, Ying-Jie,Zhou, Dongjie,Zhou, Wenjun,Nie, Zheng-Wen,Kim, Ju-Yeon,Oh, YoungJin,Lee, So-Rim,Cui, Xiang-Shun The Korean Society of Animal Reproduction and Biot 2020 한국동물생명공학회지 Vol.35 No.1
Nitric oxide (NO)-induced protein S-nitrosylation triggers mitochondrial dysfunction and was related to cell senescence. However, the exact mechanism of these damages is not clear. In the present study, to investigate the relationship between in vitro aging and NO-induced protein S-nitrosylation, oocytes were treated with sodium nitroprusside dihydrate (SNP), and the resultant S-nitrosylated proteins were detected through biotin-switch assay. The results showed that levels of protein S-nitroso thiols (SNO)s and expression of S-nitrosoglutathione reductase (GSNOR) increased, while activity and function of mitochondria were impaired during oocyte aging. Addition of SNP, a NO donor, to the oocyte culture led to accelerated oocyte aging, increased mitochondrial dysfunction and damage, apoptosis, ATP deficiency, and enhanced ROS production. These results suggested that the increased NO signal during oocyte aging in vitro, accelerated oocyte degradation due to increased protein S-nitrosylation, and ROS-related redox signaling.
In Vitro and In Vivo Studies on the Complexes of Vinpocetine with Hydroxypropyl-β-cyclodextrin
Shufang Nie,Xiaowen Fan,Ying Peng,Xingang Yang,Chao Wang,Weisan Pan 대한약학회 2007 Archives of Pharmacal Research Vol.30 No.8
The purpose of this study was to evaluate complexes of vinpocetine (VIN), a poorly water-soluble base type drug, with hydroxypropyl-β-cyclodextrin (HP-β-CD) in aqueous environment and in solid state, with or without citric acid (CA) as an acidifier of the complexation medium. The apparent stability constant (Kc) calculated by phase solubility was 282 M-1 and the complexation in solution was structurally characterized by 1H-NMR which showed VIN was likely to fit into the cyclodextrin cavity with its phenyl ring and ethyl ester bond. Solid complexes of VIN and HP-β-CD were prepared by kneading (KE), co-evaporating (CE) and freeze-drying (FD) methods. Physical mixtures were prepared for comparison. The study in the solid state included the differential scanning calorimetry (DSC), X-ray diffractometry (XRD) and infrared absorption spectroscopy (IR). From these analyses, CE and FD products were found in amorphous state, allowing to the conclusion of strong evidences of inclusion complex formation. However, the dissolution test showed that only VIN/HP-β-CD+CA complexes by CE and FD method could provide satisfying dissolution behavior (rapid, complete and lasting) when compared to that of VIN/HP-β-CD complexes. Interestingly, the addition of CA in inclusion complexes could significantly decrease the amount of HP-β-CD needed to solubilize the same amount of VIN and thereby reducing the formulation bulk. Furthermore, in-vivo study revealed that the bioavailability of VIN after oral administration to rabbits (n=6) was significantly improved by VIN/HP-β-CD+CA inclusion complex.
Yang, Ying,Nie, Wei,Yuan, Jianmin,Zhang, Bingkun,Wang, Zhong,Wu, Zhenlong,Guo, Yuming Korean Society for Biochemistry and Molecular Bion 2010 Experimental and molecular medicine Vol.42 No.11
Deregulation of endothelial nitric oxide synthase (eNOS) plays an important role in the development of multiple cardiovascular diseases. Our recent study demonstrated that genistein supplementation attenuates pulmonary arterial hypertension in broilers by restoration of endothelial function. In this study, we investigated the molecular mechanism by using broiler pulmonary arterial endothelial cells (PAECs). Our results showed that genistein stimulated a rapid phosphorylation of eNOS at $Ser^{1179}$ which was associated with activation of eNOS/NO axis. Further study indicated that the activation of eNOS was not mediated through estrogen receptors or tyrosine kinase inhibition, but via a phosphatidylinositol 3-kinase (PI3K)/Akt-dependent signaling pathway, as the eNOS activity and related NO release were largely abolished by pharmacological inhibitors of PI3K or Akt. Thus, our findings revealed a critical function of Akt in mediating genistein-stimulated eNOS activity in PAECs, partially accounting for the beneficial effects of genistein on the development of cardiovascular diseases observed in animal models.