Key Laboratory of Adolescent Health Assessment and Exercise Intervention

Shanghai, China

Key Laboratory of Adolescent Health Assessment and Exercise Intervention

Shanghai, China
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Yu F.,Key Laboratory of Adolescent Health Assessment and Exercise Intervention | Yu F.,East China Normal University | Xu B.,Key Laboratory of Adolescent Health Assessment and Exercise Intervention | Xu B.,East China Normal University | And 4 more authors.
NeuroReport | Year: 2013

Chronic administration of D-galactose simulates the changes in natural senescence and accelerates aging in animal models and has been used in aging research. The present study was undertaken to investigate the molecular mechanisms underlying the effects of exercise on learning and memory in rats with D-galactose-induced aging. The learning and memory performance in aging rats, either after exercise or without exercise, was assessed with the Morris water maze test. The effect of treadmill exercise on the expression of amyloid-β 42 and two key enzymes involved in processing of the β-amyloid precursor protein, a disintegrase and metalloprotease domain 17 and β-site amyloid precursor protein-cleaving enzyme 1, in the hippocampi of rats were monitored using real-time quantitative PCR. Moreover, oxidative stress-associated changes, including changes in superoxide dismutase activity and malondialdehyde content, in the hippocampi were assessed after exercise. Our results showed that treadmill exercise significantly improved learning and memory performance in aging rats. The behavioral changes were likely induced by repression of amyloid-β 42 protein levels, through the upregulation of a disintegrase and metalloprotease domain 17 mRNA and downregulation of β-site amyloid precursor protein-cleaving enzyme 1 mRNA, and a concomitant increase in superoxide dismutase activity and decrease in malondialdehyde content, in rat hippocampi. Our data suggest that exercise may be an effective therapy for alleviating learning and memory decline due to aging or the onset of neurodegenerative diseases.


Zhang Y.,York University | Zhang Y.,Key Laboratory of Adolescent Health Assessment and Exercise Intervention | Zhang Y.,East China Normal University | Iqbal S.,York University | And 6 more authors.
American Journal of Physiology - Cell Physiology | Year: 2013

The function Bax and/or Bak in constituting a gateway for mitochondrial apoptosis in response to apoptotic stimuli has been unequivocally demonstrated. However, recent work has suggested that Bax/Bak may have unrecognized nonapoptotic functions related to mitochondrial function in nonstressful environments. Wild-type (WT) and Bax/Bak double knockout (DKO) mice were used to determine alternative roles for Bax and Bak in mitochondrial morphology and protein import in skeletal muscle. The absence of Bax and/or Bak altered mitochondrial dynamics by regulating protein components of the organelle fission and fusion machinery. Moreover, DKO mice exhibited defective mitochondrial protein import, both into the matrix and outer membrane compartments, which was consistent with our observations of impaired membrane potential and attenuated expression of protein import machinery (PIM) components in intermyofibrillar mitochondria. Furthermore, the cytosolic chaperones heat-shock protein 90 (Hsp90) and binding immunoglobulin protein (BiP) were markedly increased with the deletion of Bax/Bak, indicating that the cytosolic environment related to protein folding may be changed in DKO mice. Interestingly, endurance training fully restored the deficiency of protein import in DKO mice, likely via the upregulation of PIM components and through improved cytosolic chaperone protein expression. Thus our results emphasize novel roles for Bax and/or Bak in mitochondrial function and provide evidence, for the first time, of a curative function of exercise training in ameliorating a condition of defective mitochondrial protein import. © 2013 the American Physiological Society.


Luo Y.-R.,Henan Normal University | Luo Y.-R.,Key Laboratory of Adolescent Health Assessment and Exercise Intervention
Advanced Materials Research | Year: 2011

Starting from regional distribution, unit distribution, enrollment distribution and other parameters, the paper makes a multi-angle and all-round analysis of the distribution of master of science in physical education (MSPE) degree programs in China, pointing out that regional balance of MSPE should pay attention to in future development. To promote the development of MSPE education, the regional enrollment should be optimized according to social needs, independent training should be maintained, and the training system should be improved. Professional degree is a type of degree specific to a certain field for those high-level professionals with competence and professionalism, and those engaged creatively in practical jobs. Professional degree education began in 1991 in China, and has developed rapidly with remarkable achievements after more than twenty years of construction. As a professional degree for the cultivation of "high-level and applied physical education professionals capable of independent sports expertise or management", master of science in physical education (MSPE), though not set for long, has developed smoothly and changed the situation of high-level and applied professional shortage. The analysis of future MSPE development from the distribution of degree programs is of special significance at present, when the structure of graduate education is being adjusted and graduate education for professional degrees being developed. © (2011) Trans Tech Publications, Switzerland.


Xu B.,Key Laboratory of Adolescent Health Assessment and Exercise Intervention | Yu F.,Key Laboratory of Adolescent Health Assessment and Exercise Intervention | Zhang X.,Key Laboratory of Adolescent Health Assessment and Exercise Intervention
Chinese Journal of Rehabilitation Medicine | Year: 2014

Objective: To explore the effects of 8-week aerobic treadmill training on expressions of β-amyloid precursor protein (APP), Tau protein and glycogen synthase kinase-3β (GSK-3β) mRNA in hippocampus of D-galactose (D-gal) Alzheimer's disease (AD) rats.Method: Sixteen male Sprague-Dawley(SD) rats were randomly divided into control group (C, n=8), exercise group(T, n=8). All rats of two groups were injected D-gal 120mg/(kg· d) in abdominal for 8 weeks to obtain AD model rats. Group T was given aerobic treadmill, 5 times a week for 8 weeks. The expression levels of APP, Tau and GSK-3β in hippocampus of all rats were inspected by real-time fluorescence quantitative RT-PCR.Result: After 8- week aerobic treadmill exercise made the expressions of APP mRNA (42%, P<0.05), Tau mRNA (45%, P<0.01) and GSK-3β (38%, P<0.05) were down-regulated significantly in hippocampus of Dgal AD rats.Conclusion: Eight- week aerobic treadmill training could made some inhibition effects on the expressions of APP and Tau mRNA in D-gal AD rats. The mechanisms might be related with the lower expression level of GSK-3β mRNA, which was down-regulated by 8 weeks aerobic treadmill exercise and would made some important regulation effects on the levels of APP and Tau protein expression. ©, 2014, China-Japan Friendship Hospital. All right reserved.


He J.,Key Laboratory of Adolescent Health Assessment and Exercise Intervention | He J.,East China Normal University | Qi Z.,Key Laboratory of Adolescent Health Assessment and Exercise Intervention | Qi Z.,East China Normal University | And 11 more authors.
Mitochondrion | Year: 2012

We investigated the biogenesis and mitochondrial antioxidant capacity of cytochrome c oxidase (COX) within the skeletal muscle under the treatments of p53 inhibitors (pifithrin, PFTα and PFTμ). Significantly, PFTμ increased mtDNA content and COX biogenesis. These changes coincided with increases in the activity and expression of manganese superoxide dismutase (MnSOD), the key antioxidant enzyme in mitochondria. Conversely, PFTα caused muscle loss, increased oxidative damage and decreased MnSOD activity in intermyofibrillar (IMF) mitochondria. Mechanically, PFTμ inhibited p53 translocation to mitochondria and thus increased its transcriptional activity for expression of synthesis of cytochrome c oxidase 2 (SCO2), an important assembly protein for COX. This study provides in vivo evidence that PFTμ, superior to PFTα, preserves muscle mass and increases mitochondrial antioxidant activity. © 2012 Elsevier B.V. and Mitochondria Research Society.


Li L.,Key Laboratory of Adolescent Health Assessment and Exercise Intervention | Li L.,East China Normal University | Men W.-W.,East China Normal University | Chang Y.-K.,National Taiwan Sport University | And 4 more authors.
PLoS ONE | Year: 2014

There is increasing evidence that acute aerobic exercise is associated with improved cognitive function. However, neural correlates of its cognitive plasticity remain largely unknown. The present study examined the effect of a session of acute aerobic exercise on working memory task-evoked brain activity as well as task performance. A within-subjects design with a counterbalanced order was employed. Fifteen young female participants (M = 19.56, SD = 0.81) were scanned using functional magnetic resonance imaging while performing a working memory task, the N-back task, both following an acute exercise session with 20 minutes of moderate intensity and a control rest session. Although an acute session of exercise did not improve behavioral performance, we observed that it had a significant impact on brain activity during the 2-back condition of the N-back task. Specifically, acute exercise induced increased brain activation in the right middle prefrontal gyrus, the right lingual gyrus, and the left fusiform gyrus as well as deactivations in the anterior cingulate cortexes, the left inferior frontal gyrus, and the right paracentral lobule. Despite the lack of an effect on behavioral measures, significant changes after acute exercise with activation of the prefrontal and occipital cortexes and deactivation of the anterior cingulate cortexes and left frontal hemisphere reflect the improvement of executive control processes, indicating that acute exercise could benefit working memory at a macro-neural level. In addition to its effects on reversing recent obesity and disease trends, our results provide substantial evidence highlighting the importance of promoting physical activity across the lifespan to prevent or reverse cognitive and neural decline. © 2014 Li et al.


Qi Z.,Key Laboratory of Adolescent Health Assessment and Exercise Intervention | Qi Z.,East China Normal University | He J.,Key Laboratory of Adolescent Health Assessment and Exercise Intervention | Su Y.,Key Laboratory of Adolescent Health Assessment and Exercise Intervention | And 10 more authors.
PLoS ONE | Year: 2011

The purpose of this study was to outline the timelines of mitochondrial function, oxidative stress and cytochrome c oxidase complex (COX) biogenesis in cardiac muscle with age, and to evaluate whether and how these age-related changes were attenuated by exercise. ICR/CD-1 mice were treated with pifithrin-μ (PFTμ), sacrificed and studied at different ages; ICR/CD-1 mice at younger or older ages were randomized to endurance treadmill running and sedentary conditions. The results showed that mRNA expression of p53 and its protein levels in mitochondria increased with age in cardiac muscle, accompanied by increased mitochondrial oxidative stress, reduced expression of COX subunits and assembly proteins, and decreased expression of most markers in mitochondrial biogenesis. Most of these age-related changes including p53 activity targeting cytochrome oxidase deficient homolog 2 (SCO2), p53 translocation to mitochondria and COX biogenesis were attenuated by exercise in older mice. PFTμ, an inhibitor blocking p53 translocation to mitochondria, increased COX biogenesis in older mice, but not in young mice. Our data suggest that physical exercise attenuates age-related changes in mitochondrial COX biogenesis and p53 activity targeting SCO2 and mitochondria, and thereby induces antisenescent and protective effects in cardiac muscle. © 2011 Qi et al.


Sun Y.,Key Laboratory of Adolescent Health Assessment and Exercise Intervention | Sun Y.,East China Normal University | Qi Z.,Key Laboratory of Adolescent Health Assessment and Exercise Intervention | Qi Z.,East China Normal University | And 10 more authors.
Free Radical Biology and Medicine | Year: 2015

Mitochondrial biogenesis refers to increased content of mitochondria, which has been shown to be promoted by aerobic exercise. During this process, oxidative stress is considered the essential initiator. Even though some studies have addressed the issue as to whether antioxidants would hamper the effects of exercise on mitochondrial biogenesis, no consensus has been achieved. Therefore, the purpose of the present study was to investigate the effects of exercise and antioxidant intervention on mitochondrial biogenesis, as well as COX biogenesis. Thirty-two clean-grade male ICR mice were randomly assigned to a control group (Con), exercise group (Ex), N-acetyl-L-cysteine group (NAC), or NAC plus exercise group (NEx). The NAC and NEx groups were injected with NAC (0.1 mg/g/2 days) intraperitoneally for 3 weeks, whereas the Con and Ex groups were administered saline for the same period of time. Mice assigned to Ex and NEx groups started exercise training 1 week before drug intervention was initiated. After 1 week of acclimatization, the mice were allowed to run at a speed of 28 m/min for 60 min, 6 days a week. The results showed that exercise training caused an increase in mRNA and protein levels of COXIV, whereas NAC intervention lowered the two so significantly that even exercise training could not reverse the effect of NAC intervention. Our data suggest that even though antioxidant intervention could alleviate oxidative damage caused by exercise, it was not necessarily beneficial for mitochondrial biogenesis. © 2015 Elsevier Inc. All rights reserved.


PubMed | Key Laboratory of Adolescent Health Assessment and Exercise Intervention
Type: Journal Article | Journal: PloS one | Year: 2011

The purpose of this study was to outline the timelines of mitochondrial function, oxidative stress and cytochrome c oxidase complex (COX) biogenesis in cardiac muscle with age, and to evaluate whether and how these age-related changes were attenuated by exercise. ICR/CD-1 mice were treated with pifithrin- (PFT), sacrificed and studied at different ages; ICR/CD-1 mice at younger or older ages were randomized to endurance treadmill running and sedentary conditions. The results showed that mRNA expression of p53 and its protein levels in mitochondria increased with age in cardiac muscle, accompanied by increased mitochondrial oxidative stress, reduced expression of COX subunits and assembly proteins, and decreased expression of most markers in mitochondrial biogenesis. Most of these age-related changes including p53 activity targeting cytochrome oxidase deficient homolog 2 (SCO2), p53 translocation to mitochondria and COX biogenesis were attenuated by exercise in older mice. PFT, an inhibitor blocking p53 translocation to mitochondria, increased COX biogenesis in older mice, but not in young mice. Our data suggest that physical exercise attenuates age-related changes in mitochondrial COX biogenesis and p53 activity targeting SCO2 and mitochondria, and thereby induces antisenescent and protective effects in cardiac muscle.


PubMed | Key Laboratory of Adolescent Health Assessment and Exercise Intervention
Type: Journal Article | Journal: Mitochondrion | Year: 2012

We investigated the biogenesis and mitochondrial antioxidant capacity of cytochrome c oxidase (COX) within the skeletal muscle under the treatments of p53 inhibitors (pifithrin, PFT and PFT). Significantly, PFT increased mtDNA content and COX biogenesis. These changes coincided with increases in the activity and expression of manganese superoxide dismutase (MnSOD), the key antioxidant enzyme in mitochondria. Conversely, PFT caused muscle loss, increased oxidative damage and decreased MnSOD activity in intermyofibrillar (IMF) mitochondria. Mechanically, PFT inhibited p53 translocation to mitochondria and thus increased its transcriptional activity for expression of synthesis of cytochrome c oxidase 2 (SCO2), an important assembly protein for COX. This study provides in vivo evidence that PFT, superior to PFT, preserves muscle mass and increases mitochondrial antioxidant activity.

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