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ABSTRACT: Closed-head injury (CHI) usually involves both physical damage of neurons and neuroinflammation. Although exercise promotes neuron repair and suppresses neuroinflammation, currently CHI patients often stay resting during the post-traumatic period. This study aimed to investigate whether and how post-injury exercise benefited the brain structure and function in CHI mice. CHI caused immediately elevated neurological severity score, rapid loss of object recognition memory, and followed by progressive location-dependent brain damages (neuronal loss and microglia activation in the cortex and hippocampus). An early exercise paradigm at moderate intensity (started 2 d post-impact and lasting for 7 or 14 days) effectively restored the object recognition memory, prevented the progressive neuronal loss and microglia activation. However, the exercise started 9 d post-impact was unable to recover recognition memory deficits. In parallel, early exercise intervention drastically promoted neurite regeneration, while late exercise intervention was much less effective. We further tested the possible involvement of brain-derived neurotrophic factor (BDNF) and MAP kinase phosphatase-1 (MKP-1) in the exercise-induced beneficial effects. Exercise gradually restored the impact-abolished hippocampal expression of BDNF and MPK-1, while oral administration of triptolide (a synthesis inhibitor of MKP-1 and an antagonist of nuclear factor-κB) before each bout of exercise blocked the exercise-restoring effects of MKP-1 and recognition memory, and the exercise-retarded neuronal loss. Although triptolide treatment alone inhibited microglia activation and maintained the neuron number, it did not recover the injury-hampered recognition memory. Taken together, moderate exercise shortly after CHI reversed the deficits in recognition memory and prevented the progression of brain injury.
The Journal of Physiology 11/2012; · 4.72 Impact Factor
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ABSTRACT: Currently, it is unclear how chronic exercise affects immunity. Mitogen-activated protein kinase (MAPK) mediates the production of proinflammatory cytokines, whereas MAPK phosphatase-1 (MKP-1) plays an essential role in intracellular homeostasis by negatively regulating macrophage MAPK activation. We hypothesized that chronic exercise might upregulate macrophage MKP-1 and thus prevent excessive inflammatory responses.
To verify this hypothesis, we compared the basal immune status and lipopolysaccharide (LPS)-evoked immune responses between sedentary and 8-wk treadmill exercise-trained male C57BL/6 mice.
Although the basal levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were undetectable in the serum of both groups, the exercised mice showed the following immune adaptations in vivo: (i) higher basal MKP-1 mRNA level in peritoneal macrophages, (ii) lower basal p38 MAPK activity and enhanced MKP-1 immunostaining in macrophages, and (iii) lower serum levels of IL-6 and TNF-α and less leukocyte infiltration into peritoneal cavity after systemic administration of LPS when compared with sedentary controls. In addition, when peritoneal macrophages isolated from exercised mice were exposed to LPS in vitro, they showed (i) accelerated MKP-1 protein expression, (ii) reduced p38 MAPK activity, and (iii) reduced cytokine secretion of IL-6, TNF-α, and monocyte chemotactic protein-1. Finally, 2 months of deconditioning completely reversed the exercise-enhanced basal MKP-1 immunostaining in macrophages and the exercise-suppressed cytokine secretion under LPS-evoked conditions.
Exercise training upregulated basal macrophage MKP-1 expression, accelerated LPS-evoked MKP-1 up-regulation, and affected LPS-evoked immune responses in mice.
Medicine and science in sports and exercise 12/2010; 42(12):2173-9. · 3.71 Impact Factor
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ABSTRACT: To investigate the cytotoxicity of triamcinolone acetonide (TA) suspensions to corneal endothelial cells (CECs).
Department of Ophthalmology, Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
New Zealand white rabbit CECs were exposed for 1 minute to balanced salt solution (BSS); commercial TA suspension (cTA); vehicle-removed TA (-vTA); pure vehicle (V); 1/10 dilutions of cTA, -vTA, or V in BSS; or benzyl alcohol (BA) (cTA preservative) 9 mg/mL. Corneal endothelial cell toxicity was assessed by light microscopy (trypan blue staining) and transmission electron microscopy. The effects of 3-, 10-, or 30-minute exposures to 1/10 cTA, 1/10 -vTA, or V were also investigated.
One-minute exposures to -vTA or 1/10 -vTA did not damage CECs; however, cTA, V, or 1/10 dilutions of cTA or V caused damage and cells exposed to BA showed severe ultrastructural damage/lysis. A 30-minute exposure to 1/10 -vTA did not cause significant cell damage, whereas 3- to 30-minute exposures to 1/10 cTA or V showed significant time-dependent cytotoxicity.
Commercial TA suspension was cytotoxic to cultured rabbit CECs because of the preservative, BA, in the vehicle. Because 1/10 -vTA appeared to be safe for up to 30 minutes of exposure, use of 1/10 dilutions of vehicle-removed TA is suggested to help surgeons visualize prolapsed vitreous during anterior vitrectomy in complicated cataract surgeries.
Journal of Cataract [?] Refractive Surgery 10/2006; 32(9):1549-55. · 2.26 Impact Factor
