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学者姓名:刘健康

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Oxidative damage of mitochondrial respiratory chain in different organs of a rat model of diet-induced obesity SCIE PubMed Scopus
期刊论文 | 2018 , 57 (5) , 1957-1967 | EUROPEAN JOURNAL OF NUTRITION
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Abstract :

Mitochondrial dysfunction plays an important role in the development of obesity and obesity-associated metabolic diseases. In this study, we dynamically observed the characteristics of mitochondrial damage in a rat model of diet-induced obesity (DIO). From the 2nd to the 10th week, animals were killed every 2 weeks and the heart, liver, kidney, and testicular tissues were harvested. Mitochondria were isolated and the activities of respiratory chain complexes I, II, III, and IV as well as the 8-Hydroxy-2-deoxy Guanosine content were determined. Reactive oxygen species and malondialdehyde were measured. Mitochondrial damages were observed in the heart and liver of DIO and DR rats, and the damages occurred later in DR group than that in DIO group. The mitochondrial membrane potential of heart and liver decreased in DIO and DR groups. The activity of the heart mitochondria complexes I, III, and IV (composing NADH oxidative respiratory) was higher in the early stage of DIO and lower in the end of week 10. The higher activity of the liver complexes I, III, and IV was found until the end of week 10 in DIO and DR groups, accompanied with enhanced oxidative stress. Besides, mitochondrial DNA damages were observed in all tissues. In DIO rats, the heart mitochondrial dysfunction occurred first and the liver presented the strongest compensatory ability against oxidative stress.

Keyword :

Obesity Respiratory chain Mitochondria Complex Oxidative stress

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GB/T 7714 Yu, Hai-Tao , Fu, Xiao-Yi , Liang, Bing et al. Oxidative damage of mitochondrial respiratory chain in different organs of a rat model of diet-induced obesity [J]. | EUROPEAN JOURNAL OF NUTRITION , 2018 , 57 (5) : 1957-1967 .
MLA Yu, Hai-Tao et al. "Oxidative damage of mitochondrial respiratory chain in different organs of a rat model of diet-induced obesity" . | EUROPEAN JOURNAL OF NUTRITION 57 . 5 (2018) : 1957-1967 .
APA Yu, Hai-Tao , Fu, Xiao-Yi , Liang, Bing , Wang, Shuang , Liu, Jian-Kang , Wang, Shu-Ran et al. Oxidative damage of mitochondrial respiratory chain in different organs of a rat model of diet-induced obesity . | EUROPEAN JOURNAL OF NUTRITION , 2018 , 57 (5) , 1957-1967 .
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SIRT3/SOD2 maintains osteoblast differentiation and bone formation by regulating mitochondrial stress SCIE PubMed Scopus
期刊论文 | 2018 , 25 (2) , 229-240 | CELL DEATH AND DIFFERENTIATION
WoS CC Cited Count: 5
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Abstract :

Recent studies have revealed robust metabolic changes during cell differentiation. Mitochondria, the organelles where many vital metabolic reactions occur, may play an important role. Here, we report the involvement of SIRT3-regulated mitochondrial stress in osteoblast differentiation and bone formation. In both the osteoblast cell line MC3T3-E1 and primary calvarial osteoblasts, robust mitochondrial biogenesis and supercomplex formation were observed during differentiation, accompanied by increased ATP production and decreased mitochondrial stress. Inhibition of mitochondrial activity or an increase in mitochondrial superoxide production significantly suppressed osteoblast differentiation. During differentiation, SOD2 was specifically induced to eliminate excess mitochondrial superoxide and protein oxidation, whereas SIRT3 expression was increased to enhance SOD2 activity through deacetylation of K68. Both SOD2 and SIRT3 knockdown resulted in suppression of differentiation. Meanwhile, mice deficient in SIRT3 exhibited obvious osteopenia accompanied by osteoblast dysfunction, whereas overexpression of SOD2 or SIRT3 improved the differentiation capability of primary osteoblasts derived from SIRT3-deficient mice. These results suggest that SIRT3/SOD2 is required for regulating mitochondrial stress and plays a vital role in osteoblast differentiation and bone formation.

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GB/T 7714 Gao, Jing , Feng, Zhihui , Wang, Xueqiang et al. SIRT3/SOD2 maintains osteoblast differentiation and bone formation by regulating mitochondrial stress [J]. | CELL DEATH AND DIFFERENTIATION , 2018 , 25 (2) : 229-240 .
MLA Gao, Jing et al. "SIRT3/SOD2 maintains osteoblast differentiation and bone formation by regulating mitochondrial stress" . | CELL DEATH AND DIFFERENTIATION 25 . 2 (2018) : 229-240 .
APA Gao, Jing , Feng, Zhihui , Wang, Xueqiang , Zeng, Mengqi , Liu, Jing , Han, Shujun et al. SIRT3/SOD2 maintains osteoblast differentiation and bone formation by regulating mitochondrial stress . | CELL DEATH AND DIFFERENTIATION , 2018 , 25 (2) , 229-240 .
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The Physiological Functions of Phytosterols and Their Underlying Mechanism of Regulating Mitochondria SCIE
期刊论文 | 2018 , 45 (12) , 1240-1249 | PROGRESS IN BIOCHEMISTRY AND BIOPHYSICS
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Abstract :

Phytosterols are a type of bioactive substances widely found in plants and have broad application prospects in food, medicine, cosmetics and other fields. Phytosterols, as cholesterol analogues, can inhibit the absorption of cholesterol in the intestine and decrease serum cholesterol level and thus reduce the risk of cardiovascular diseases. In addition, phytosterols have many other functions such as cancer suppression, anti-inflammation or anti-fever, anti-oxidation and hormone-like effects. In-depth exploration of the subcellular and molecular mechanism of phytosterols' biological functions contributes to the full development of the application value of phytosterols. Mitochondria are the most important sites for cellular energy metabolism. Cholesterol metabolism, cancer cell proliferation and apoptosis, oxidative stress, and inflammatory response are all closely related to mitochondrial function. Recent studies have suggested that phytosterols can regulate mitochondrial function in various models, which potentially may be a pivotal mechanism underlying phytosterols' various biological functions. This article will first summarize the biological functions of phytosterols and then discuss its mitochondria-related regulatory mechanisms in detail, hoping to provide frontier insights and progress report for researchers in the field as well as to provide reference for the application of phytosterols.

Keyword :

antioxidase anticancer beta-sitosterol LDL-C mitochondrial membrane potential

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GB/T 7714 Lou Jing , Cui Ya-Juan , Liu Jian-Kang et al. The Physiological Functions of Phytosterols and Their Underlying Mechanism of Regulating Mitochondria [J]. | PROGRESS IN BIOCHEMISTRY AND BIOPHYSICS , 2018 , 45 (12) : 1240-1249 .
MLA Lou Jing et al. "The Physiological Functions of Phytosterols and Their Underlying Mechanism of Regulating Mitochondria" . | PROGRESS IN BIOCHEMISTRY AND BIOPHYSICS 45 . 12 (2018) : 1240-1249 .
APA Lou Jing , Cui Ya-Juan , Liu Jian-Kang , Zhao Lin . The Physiological Functions of Phytosterols and Their Underlying Mechanism of Regulating Mitochondria . | PROGRESS IN BIOCHEMISTRY AND BIOPHYSICS , 2018 , 45 (12) , 1240-1249 .
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Molecular Mechanisms for the Coupling of Endocytosis to Exocytosis in Neurons SCIE PubMed Scopus
期刊论文 | 2017 , 10 | FRONTIERS IN MOLECULAR NEUROSCIENCE | IF: 3.902
WoS CC Cited Count: 8
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Abstract :

Neuronal communication and brain function mainly depend on the fundamental biological events of neurotransmission, including the exocytosis of presynaptic vesicles (SVs) for neurotransmitter release and the subsequent endocytosis for SV retrieval. Neurotransmitters are released through the Ca2+-and SNARE-dependent fusion of SVs with the presynaptic plasma membrane. Following exocytosis, endocytosis occurs immediately to retrieve SV membrane and fusion machinery for local recycling and thus maintain the homeostasis of synaptic structure and sustained neurotransmission. Apart from the general endocytic machinery, recent studies have also revealed the involvement of SNARE proteins (synaptobrevin, SNAP25 and syntaxin), synaptophysin, Ca2+/ calmodulin, and members of the synaptotagmin protein family (Syt1, Syt4, Syt7 and Syt11) in the balance and tight coupling of exo-endocytosis in neurons. Here, we provide an overview of recent progress in understanding how these neuronspecific adaptors coordinate to ensure precise and efficient endocytosis during neurotransmission.

Keyword :

calmodulin endocytosis synaptotagmin vesicle recycling SNARE exocytosis

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GB/T 7714 Xie, Zhenli , Long, Jiangang , Liu, Jiankang et al. Molecular Mechanisms for the Coupling of Endocytosis to Exocytosis in Neurons [J]. | FRONTIERS IN MOLECULAR NEUROSCIENCE , 2017 , 10 .
MLA Xie, Zhenli et al. "Molecular Mechanisms for the Coupling of Endocytosis to Exocytosis in Neurons" . | FRONTIERS IN MOLECULAR NEUROSCIENCE 10 (2017) .
APA Xie, Zhenli , Long, Jiangang , Liu, Jiankang , Chai, Zuying , Kang, Xinjiang , Wang, Changhe . Molecular Mechanisms for the Coupling of Endocytosis to Exocytosis in Neurons . | FRONTIERS IN MOLECULAR NEUROSCIENCE , 2017 , 10 .
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Oleuropein, unexpected benefits! SCIE PubMed Scopus
期刊论文 | 2017 , 8 (11) , 17409-17409 | ONCOTARGET
WoS CC Cited Count: 3
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Keyword :

oleuropein benefits

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GB/T 7714 Sun, Wenyan , Frost, Bess , Liu, Jiankang . Oleuropein, unexpected benefits! [J]. | ONCOTARGET , 2017 , 8 (11) : 17409-17409 .
MLA Sun, Wenyan et al. "Oleuropein, unexpected benefits!" . | ONCOTARGET 8 . 11 (2017) : 17409-17409 .
APA Sun, Wenyan , Frost, Bess , Liu, Jiankang . Oleuropein, unexpected benefits! . | ONCOTARGET , 2017 , 8 (11) , 17409-17409 .
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Neurodegenerative Disease Related Proteins Have Negative Effects on SNARE-Mediated Membrane Fusion in Pathological Confirmation SCIE PubMed Scopus
期刊论文 | 2017 , 10 | FRONTIERS IN MOLECULAR NEUROSCIENCE | IF: 3.902
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Keyword :

single molecule biophysics technology neurotransmitter release membrane fusion neurodegenerative diseases SNARE

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GB/T 7714 Hou, Chen , Wang, Yongyao , Liu, Jiankang et al. Neurodegenerative Disease Related Proteins Have Negative Effects on SNARE-Mediated Membrane Fusion in Pathological Confirmation [J]. | FRONTIERS IN MOLECULAR NEUROSCIENCE , 2017 , 10 .
MLA Hou, Chen et al. "Neurodegenerative Disease Related Proteins Have Negative Effects on SNARE-Mediated Membrane Fusion in Pathological Confirmation" . | FRONTIERS IN MOLECULAR NEUROSCIENCE 10 (2017) .
APA Hou, Chen , Wang, Yongyao , Liu, Jiankang , Wang, Changhe , Long, Jiangang . Neurodegenerative Disease Related Proteins Have Negative Effects on SNARE-Mediated Membrane Fusion in Pathological Confirmation . | FRONTIERS IN MOLECULAR NEUROSCIENCE , 2017 , 10 .
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Thinned young apple polysaccharide improves hepatic metabolic disorder in high-fat diet-induced obese mice by activating mitochondrial respiratory functions SCIE Scopus
期刊论文 | 2017 , 33 , 396-407 | JOURNAL OF FUNCTIONAL FOODS | IF: 3.47
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Abstract :

Apple polysaccharides have been previously demonstrated to have beneficial effects on hepatic metabolic functions. Approximately 1.9 million tons of young apples are thinned and abandoned annually in China, and whether the polysaccharide derived from these thinned young apples has metabolic benefits lacks evidence. Thinned young apple polysaccharide (TYAP) has been investigated in high fat diet (HFD)induced obese mice for its effect on metabolic disorder. Water-soluble TYAP was isolated from thinned young apples and chemically characterized. TYAP administration at dosages of 400 mg/kg/day and 800 mg/kg/day significantly rescued HFD-induced hepatic metabolic impairment, reduced body weight gain, and ameliorated hepatic oxidative stress induced by HFD. In a palmitate-loaded HepG2 cell model, TYAP protected the cells from palmitate-induced insulin resistance and viability loss, suppressed mitochondrial ROS and improved the mitochondrial respiratory function impaired by palmitate. These findings suggest that TYAP could successfully attenuate obesity-associated hepatic metabolic disorder possibly by activating the hepatic mitochondrial respiratory function. (C) 2017 Published by Elsevier Ltd.

Keyword :

High-fat diet Oxidative stress Thinned young apple polysaccharide Hepatic metabolic disorder Mitochondrial respiratory function

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GB/T 7714 Chen, Lei , Yang, Xi , Liu, Run et al. Thinned young apple polysaccharide improves hepatic metabolic disorder in high-fat diet-induced obese mice by activating mitochondrial respiratory functions [J]. | JOURNAL OF FUNCTIONAL FOODS , 2017 , 33 : 396-407 .
MLA Chen, Lei et al. "Thinned young apple polysaccharide improves hepatic metabolic disorder in high-fat diet-induced obese mice by activating mitochondrial respiratory functions" . | JOURNAL OF FUNCTIONAL FOODS 33 (2017) : 396-407 .
APA Chen, Lei , Yang, Xi , Liu, Run , Liu, Lei , Zhao, Daina , Liu, Jiankang et al. Thinned young apple polysaccharide improves hepatic metabolic disorder in high-fat diet-induced obese mice by activating mitochondrial respiratory functions . | JOURNAL OF FUNCTIONAL FOODS , 2017 , 33 , 396-407 .
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Oleuropein improves mitochondrial function to attenuate oxidative stress by activating the Nrf2 pathway in the hypothalamic paraventricular nucleus of spontaneously hypertensive rats SCIE PubMed Scopus
期刊论文 | 2017 , 113 , 556-566 | NEUROPHARMACOLOGY | IF: 4.249
WoS CC Cited Count: 13 SCOPUS Cited Count: 14
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Abstract :

Hypertension is associated with increased reactive oxygen species (ROS) production in the paraventricular nucleus (PVN) of the hypothalamus. Oleuropein (OL) has a variety of biochemical roles, including antihypertensive and antioxidative functions. However, there have been few reports on the effects of OL on oxidative stress in the PVN on hypertension. In spontaneously hypertensive rats (SHR), eight-week administration of 60 mg/kg/day of OL significantly reduced blood pressure, pro inflammatory cytokines and the expression of components of the renin-angiotensin system (RAS) compared with SHR rats treated with saline. Concomitantly, OL inhibited superoxide, and increased the antioxidant defense system in the PVN of SHR. We also found that OL increased mitochondria] biogenesis through mtDNA, PGC-1 alpha, Complex II and Complex IV expression and regulated mitochondrial dynamics through the fusion-related protein Mfn2 and fision-related protein DRP1 to attenuate mitochondrial impairment. Furthermore, the phase II enzyme levels of Nrf2 and its downstream proteins NQO-1 and HO-1 were all markedly increased in the PVN of the OL-treated SHR group compared with the saline treated SHR rats. Our findings demonstrate that OL administration can protect the PVN of the hypothalamus from oxidative stress by improving mitochondrial function through the activation of the Nrf2-mediated signaling pathway. (C) 2016 Elsevier Ltd. All rights reserved.

Keyword :

Oleuropein Hypertension Oxidative stress Mitochondria Nrf2

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GB/T 7714 Sun, Wenyan , Wang, Xin , Hou, Chen et al. Oleuropein improves mitochondrial function to attenuate oxidative stress by activating the Nrf2 pathway in the hypothalamic paraventricular nucleus of spontaneously hypertensive rats [J]. | NEUROPHARMACOLOGY , 2017 , 113 : 556-566 .
MLA Sun, Wenyan et al. "Oleuropein improves mitochondrial function to attenuate oxidative stress by activating the Nrf2 pathway in the hypothalamic paraventricular nucleus of spontaneously hypertensive rats" . | NEUROPHARMACOLOGY 113 (2017) : 556-566 .
APA Sun, Wenyan , Wang, Xin , Hou, Chen , Yang, Liang , Li, Hongbao , Guo, Jing et al. Oleuropein improves mitochondrial function to attenuate oxidative stress by activating the Nrf2 pathway in the hypothalamic paraventricular nucleus of spontaneously hypertensive rats . | NEUROPHARMACOLOGY , 2017 , 113 , 556-566 .
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The regulatory roles of O-GlcNAcylation in mitochondrial homeostasis and metabolic syndrome. PubMed
期刊论文 | 2016 , 50 (10) , 1080-1088 | Free radical research | IF: 3.188
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Nutrients excess is one of the leading causes of metabolic syndrome globally. Protein post-translational O-GlcNAc modification has been recognized as an essential nutrient sensor of the cell. Emerging studies suggest that O-GlcNAcylation lies at the core linking nutritional stress to insulin resistance. Mitochondria are the major site for ATP production in most eukaryotes. Mitochondrial dysfunction and oxidative stress have long been considered as an important mechanism underlying insulin resistance. The metabolic process is under the influence of environmental and nutritional factors, thus sensing and transducing nutritional signals sit at the pivot of metabolism control. For a long time little was known about O-GlcNAcylation within mitochondria since mitochondrial O-GlcNAcylation was regarded rare. Recent findings have demonstrated that O-GlcNAcylation is widely spread among mitochondrial proteins, and that mitochondrial function and oxidative stress both can be regulated by O-GlcNAcylation, particularly under diabetic circumstances.

Keyword :

mitochondria nutrient sensing insulin resistance oxidative stress O-GlcNAcylation

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GB/T 7714 Zhao Lin , Feng Zhihui , Yang Xiaoyong et al. The regulatory roles of O-GlcNAcylation in mitochondrial homeostasis and metabolic syndrome. [J]. | Free radical research , 2016 , 50 (10) : 1080-1088 .
MLA Zhao Lin et al. "The regulatory roles of O-GlcNAcylation in mitochondrial homeostasis and metabolic syndrome." . | Free radical research 50 . 10 (2016) : 1080-1088 .
APA Zhao Lin , Feng Zhihui , Yang Xiaoyong , Liu Jiankang . The regulatory roles of O-GlcNAcylation in mitochondrial homeostasis and metabolic syndrome. . | Free radical research , 2016 , 50 (10) , 1080-1088 .
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Molecular Architecture of Contactin-associated Protein-like 2 (CNTNAP2) and Its Interaction with Contactin 2 (CNTN2). PubMed
期刊论文 | 2016 , 291 (46) , 24133-24147 | The Journal of biological chemistry
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Contactin-associated protein-like 2 (CNTNAP2) is a large multidomain neuronal adhesion molecule implicated in a number of neurological disorders, including epilepsy, schizophrenia, autism spectrum disorder, intellectual disability, and language delay. We reveal here by electron microscopy that the architecture of CNTNAP2 is composed of a large, medium, and small lobe that flex with respect to each other. Using epitope labeling and fragments, we assign the F58C, L1, and L2 domains to the large lobe, the FBG and L3 domains to the middle lobe, and the L4 domain to the small lobe of the CNTNAP2 molecular envelope. Our data reveal that CNTNAP2 has a very different architecture compared with neurexin 1α, a fellow member of the neurexin superfamily and a prototype, suggesting that CNTNAP2 uses a different strategy to integrate into the synaptic protein network. We show that the ectodomains of CNTNAP2 and contactin 2 (CNTN2) bind directly and specifically, with low nanomolar affinity. We show further that mutations in CNTNAP2 implicated in autism spectrum disorder are not segregated but are distributed over the whole ectodomain. The molecular shape and dimensions of CNTNAP2 place constraints on how CNTNAP2 integrates in the cleft of axo-glial and neuronal contact sites and how it functions as an organizing and adhesive molecule.

Keyword :

synapse synaptic organizer neuropsychiatric disorders protein-protein interaction structural biology contactin-associated protein like contactin single particle analysis cell adhesion cell surface receptor

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GB/T 7714 Lu Zhuoyang , Reddy M V V V Sekhar , Liu Jianfang et al. Molecular Architecture of Contactin-associated Protein-like 2 (CNTNAP2) and Its Interaction with Contactin 2 (CNTN2). [J]. | The Journal of biological chemistry , 2016 , 291 (46) : 24133-24147 .
MLA Lu Zhuoyang et al. "Molecular Architecture of Contactin-associated Protein-like 2 (CNTNAP2) and Its Interaction with Contactin 2 (CNTN2)." . | The Journal of biological chemistry 291 . 46 (2016) : 24133-24147 .
APA Lu Zhuoyang , Reddy M V V V Sekhar , Liu Jianfang , Kalichava Ana , Liu Jiankang , Zhang Lei et al. Molecular Architecture of Contactin-associated Protein-like 2 (CNTNAP2) and Its Interaction with Contactin 2 (CNTN2). . | The Journal of biological chemistry , 2016 , 291 (46) , 24133-24147 .
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