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RISS 인기검색어
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- 저자 : Zhirui Fang (검색결과 3 건)
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Chunxiao Li,Lu Chen,Min Song,Zhirui Fang,Lusha Zhang,Joel Wake Coffie,Liyuan Zhang,Lulu Ma,Qianyi Wang,Wenjie Yang,Leyu Fang,Shaoxia Wang,Xiumei Gao,Hong Wang 대한약학회 2020 Archives of Pharmacal Research Vol.43 No.8
Acute myocardial infarction (AMI) resultsin irreversible cardiac cell damage or death because ofdecreased blood fl ow to the heart. Apoptosis plays an importantrole in the process of tissue damage after myocardialinfarction (MI), which has pathological and therapeuticimplications. Ferulic acid (FA) is a phenolic acid endowedwith strong antioxidative and cytoprotective activities. Thepresent study aimed to investigate whether FA protectscardiomyocytes from apoptosis by regulating autophagy,which is a cellular self-digestion process, and one of thefi rst lines of defense against oxidative stress. Apoptosis wasinduced by TNF-α (10 ng/mL) and cycloheximide (CHX,5 μg/mL) in rat H9c2 cardiomyocytes. FA-inhibited TNF-α/CHX-induced apoptosis was determined by the quantifi cationof TUNEL-positive cells, and the eff ect was associatedwith decreased ROS production and inhibited caspase3activation. FA treatment enhanced autophagy and increasedautophagy-associated protein expression, leading to an inhibitionof mTOR signaling. When co-treated with 3-methyladenine(3-MA), an autophagy inhibitor, the anti-apoptoticeff ect of FA was attenuated. In an in vivo mouse MI model,FA treatment decreased the apoptotic cell number, reducedinfarct size, and improved cardiac performance, as determinedby histological and echocardiographic assessments. Taken collectively, these results suggest that FA could protectcardiomyocytes from apoptosis by enhancing autophagy.
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( Fangmin Xu ),( Pengkai Zou ),( Haiquan Wang ),( Haiyan Cao ),( Xin Fang ),( Zhirui Hu ) 한국인터넷정보학회 2020 KSII Transactions on Internet and Information Syst Vol.14 No.12
In a device-to-device (D2D) underlaid cellular network, there exist two types of co-channel interference. One type is inter-layer interference caused by spectrum reuse between D2D transmitters and cellular users (CUEs). Another type is intra-layer interference caused by spectrum sharing among D2D pairs. To mitigate the inter-layer interference, we first derive the interference limited area (ILA) to protect the coverage probability of cellular users by modeling D2D users’ location as a Poisson point process, where a D2D transmitter is allowed to reuse the spectrum of the CUE only if the D2D transmitter is outside the ILA of the CUE. To coordinate the intra-layer interference, the spectrum sharing criterion of D2D pairs is derived based on the (signal-to-interference ratio) SIR requirement of D2D communication. Based on this criterion, D2D pairs are allowed to share the spectrum when one D2D pair is far from another sufficiently. Furthermore, to maximize the energy efficiency of the system, a resource allocation scheme is proposed according to weighted graph coloring theory and the proposed ILA restriction. Simulation results show that our proposed scheme provides significant performance gains over the conventional scheme and the random allocation scheme.
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Ginsenoside Rg1 alleviates A deposition by inhibiting NADPH oxidase 2 activation in APP/PS1 mice
Han Zhang,Yong Su,Zhenghao Sun,Ming Chen,Yuli Han,Yan Li,Xianan Dong,Shixin Ding,Zhirui Fang,Weiping Li,Weizu Li 고려인삼학회 2021 Journal of Ginseng Research Vol.45 No.6
Background: Ginsenoside Rg1 (Rg1), an active ingredient in ginseng, may be a potential agent for thetreatment of Alzheimer’s disease (AD). However, the protective effect of Rg1 on neurodegeneration in ADand its mechanism of action are still incompletely understood. Methods: Wild type (WT) and APP/PS1 AD mice, from 6 to 9 months old, were used in the experiment. The open field test (OFT) and Morris water maze (MWM) were used to detect behavioral changes. Neuronal damage was assessed by hematoxylin and eosin (H&E) and Nissl staining. Immunofluorescence,western blotting, and quantitative real-time polymerase chain reaction (q-PCR) were used toexamine postsynaptic density 95 (PSD95) expression, amyloid beta (Ab) deposition, Tau and phosphorylatedTau (p-Tau) expression, reactive oxygen species (ROS) production, and NAPDH oxidase 2(NOX2) expression. Results: Rg1 treatment for 12 weeks significantly ameliorated cognitive impairments and neuronaldamage and decreased the p-Tau level, amyloid precursor protein (APP) expression, and Ab generation inAPP/PS1 mice. Meanwhile, Rg1 treatment significantly decreased the ROS level and NOX2 expression inthe hippocampus and cortex of APP/PS1 mice. Conclusions: Rg1 alleviates cognitive impairments, neuronal damage, and reduce Ab deposition byinhibiting NOX2 activation in APP/PS1 mice.
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