Background: The physiological and biochemical demands of intense exercise elicit both muscle-based and systemic responses. The main adaptations to endurance exercise include the correction of electrolyte imbalance, a ...Background: The physiological and biochemical demands of intense exercise elicit both muscle-based and systemic responses. The main adaptations to endurance exercise include the correction of electrolyte imbalance, a decrease in glycogen storage and the increase of oxidative stress, intestinal permeability, muscle damage, and systemic inflammatory response. Adaptations to exercise might be influenced by the gut microbiota, which plays an important role in the production, storage, and expenditure of energy obtained from the diet as well as in inflammation,redox reactions, and hydration status.Methods: A systematic and comprehensive search of electronic databases, including MEDLINE, Scopus, Clinical Trials.gov, Science Direct,Springer Link, and EMBASE was done. The search process was completed using the keywords: "endurance", "exercise", "immune response","microbiota", "nutrition", and "probiotics".Results: Reviewed literature supports the hypothesis that intestinal microbiota might be able to provide a measureable, effective marker of an athlete's immune function and that microbial composition analysis might also be sensitive enough to detect exercise-induced stress and metabolic disorders. The review also supports the hypothesis that modifying the microbiota through the use of probiotics could be an important therapeutic tool to improve athletes' overall general health, performance, and energy availability while controlling inflammation and redox levels.Conclusion: The present review provides a comprehensive overview of how gut microbiota may have a key role in controlling the oxidative stress and inflammatory responses as well as improving metabolism and energy expenditure during intense exercise.展开更多
A consistent association has been observed between leukocyte telomere length(LTL)and atherosclerosis,but the mechanisms underlying these associations are still not well understood.Premature biology aging was evident i...A consistent association has been observed between leukocyte telomere length(LTL)and atherosclerosis,but the mechanisms underlying these associations are still not well understood.Premature biology aging was evident in atherosclerotic plaques,characterized by reduced cell proliferation,irreversible growth arrest and apoptosis,and telomere attrition.As atherosclerosis is a state of chronic low-grade inflammation and increased oxidative stress,shortened LTL in patients with atherosclerosis might stem from the two sources,one is an accelerated rate in hematopoietic stem cells(HSCs)replication to replace leukocytes consumed in the inflammatory process,and another is the increase in the loss of telomere repeats per replication.Thus,diminished HSC reserves at birth and age-dependent telomere attrition afterward are mirrored in shortened LTL during the adulthood.In addition,the inter-individual variation of LTL in the general population can be partly explained by genetic factors regulating telomere maintenance and the rate of HSCs replication.Atherosclerosis is an aging-related disease,and practically all humans develop atherosclerosis if they live long enough.Here we overview the potential roles of LTL dynamics in the imbalance between injurious oxidative stress/inflammation and endothelial repair during the pathogenesis of age-related atherosclerosis,and discuss the possibility that preventing accelerated cellular senescence is a potential target in prevention of atherosclerosis.展开更多
Ischemia occurs in diabetic retinopathy with neuronal loss, edema, glial cell reactivity and oxidative stress. Epacs, consisting of Epac 1 and Epac2, are cAMP mediators playing important roles in maintenance of endoth...Ischemia occurs in diabetic retinopathy with neuronal loss, edema, glial cell reactivity and oxidative stress. Epacs, consisting of Epac 1 and Epac2, are cAMP mediators playing important roles in maintenance of endothelial barrier and neuronal functions To investigate the roles of Epacs in the pathogenesis of ischemic retinopathy, transient middle cerebral artery occlusion （tMCAO） was performed on Epacl-deficient （Epacl-/- ） mice, Epac2-deficient （Epac2-/-） mice, and their wild type counter-parts （Epacl＋/＋ and Epac2＋/＋）. Two-hour occlusion and 22-hour reperfusion were conducted to induce ischemia/reperfusion injury to the retina. After tMCAO, the contralateral retinae displayed similar morphology between different genotypes. Neu-ronal loss, retinal edema and increase in immunoreactivity for aquaporin 4 （AQP4）, glial fibrillary acidic protein （GFAP）, peroxiredoxin 6 （Prx6） were observed in ipsilateral retinae. Epac2 / ipsilateral retinae showed more neuronal loss in retinal ganglion cell layer, increased retinal thickness and stronger immunostaining of AQP4, GFAP, and Prx6 than those of Epac2＋/＋. However, Epacl-/- ipsilateral retinae displayed similar pathology as those in Epacl＋/＋ mice. Our observations suggest that Epac2-deficiency led to more severe ischemic retinopathy after retinal ischemia/reperfusion injury.展开更多
文摘Background: The physiological and biochemical demands of intense exercise elicit both muscle-based and systemic responses. The main adaptations to endurance exercise include the correction of electrolyte imbalance, a decrease in glycogen storage and the increase of oxidative stress, intestinal permeability, muscle damage, and systemic inflammatory response. Adaptations to exercise might be influenced by the gut microbiota, which plays an important role in the production, storage, and expenditure of energy obtained from the diet as well as in inflammation,redox reactions, and hydration status.Methods: A systematic and comprehensive search of electronic databases, including MEDLINE, Scopus, Clinical Trials.gov, Science Direct,Springer Link, and EMBASE was done. The search process was completed using the keywords: "endurance", "exercise", "immune response","microbiota", "nutrition", and "probiotics".Results: Reviewed literature supports the hypothesis that intestinal microbiota might be able to provide a measureable, effective marker of an athlete's immune function and that microbial composition analysis might also be sensitive enough to detect exercise-induced stress and metabolic disorders. The review also supports the hypothesis that modifying the microbiota through the use of probiotics could be an important therapeutic tool to improve athletes' overall general health, performance, and energy availability while controlling inflammation and redox levels.Conclusion: The present review provides a comprehensive overview of how gut microbiota may have a key role in controlling the oxidative stress and inflammatory responses as well as improving metabolism and energy expenditure during intense exercise.
文摘A consistent association has been observed between leukocyte telomere length(LTL)and atherosclerosis,but the mechanisms underlying these associations are still not well understood.Premature biology aging was evident in atherosclerotic plaques,characterized by reduced cell proliferation,irreversible growth arrest and apoptosis,and telomere attrition.As atherosclerosis is a state of chronic low-grade inflammation and increased oxidative stress,shortened LTL in patients with atherosclerosis might stem from the two sources,one is an accelerated rate in hematopoietic stem cells(HSCs)replication to replace leukocytes consumed in the inflammatory process,and another is the increase in the loss of telomere repeats per replication.Thus,diminished HSC reserves at birth and age-dependent telomere attrition afterward are mirrored in shortened LTL during the adulthood.In addition,the inter-individual variation of LTL in the general population can be partly explained by genetic factors regulating telomere maintenance and the rate of HSCs replication.Atherosclerosis is an aging-related disease,and practically all humans develop atherosclerosis if they live long enough.Here we overview the potential roles of LTL dynamics in the imbalance between injurious oxidative stress/inflammation and endothelial repair during the pathogenesis of age-related atherosclerosis,and discuss the possibility that preventing accelerated cellular senescence is a potential target in prevention of atherosclerosis.
基金supported by the Research Grants Council of Hong Kong(RGC)HKU 764008M to Sookja Kim Chung
文摘Ischemia occurs in diabetic retinopathy with neuronal loss, edema, glial cell reactivity and oxidative stress. Epacs, consisting of Epac 1 and Epac2, are cAMP mediators playing important roles in maintenance of endothelial barrier and neuronal functions To investigate the roles of Epacs in the pathogenesis of ischemic retinopathy, transient middle cerebral artery occlusion （tMCAO） was performed on Epacl-deficient （Epacl-/- ） mice, Epac2-deficient （Epac2-/-） mice, and their wild type counter-parts （Epacl＋/＋ and Epac2＋/＋）. Two-hour occlusion and 22-hour reperfusion were conducted to induce ischemia/reperfusion injury to the retina. After tMCAO, the contralateral retinae displayed similar morphology between different genotypes. Neu-ronal loss, retinal edema and increase in immunoreactivity for aquaporin 4 （AQP4）, glial fibrillary acidic protein （GFAP）, peroxiredoxin 6 （Prx6） were observed in ipsilateral retinae. Epac2 / ipsilateral retinae showed more neuronal loss in retinal ganglion cell layer, increased retinal thickness and stronger immunostaining of AQP4, GFAP, and Prx6 than those of Epac2＋/＋. However, Epacl-/- ipsilateral retinae displayed similar pathology as those in Epacl＋/＋ mice. Our observations suggest that Epac2-deficiency led to more severe ischemic retinopathy after retinal ischemia/reperfusion injury.
