AIM:To investigate the age-related alterations of cytoskeleton system in liver Kupffer cell and their relation to the changed phagocytic function.METHODS: The phagocytic function of Kupffer cells from rats of various ages (6mo, 12mo,18mo and 24mo) were quantitatively evaluated by phagocytosis of polystyrene beads. The actin distribution and measurement of Kupffer cell were determined by a phalloidin-TRITC method; and the myosin and vimentin distribution and measurement with indirect immunochemical staining.RESULTS: Aging resulted in significant alterations of actin, myosin and vimentin distributions and reductions in Kupffer cell; the 3 cytoskeleton components of 24-mo-old Kupffer cell were significantly decreased to 68.0%, 84.9% and 75.5%, respectively of these of 6-mo-old Kupffer cell(P < 0.01,0.01 and 0.01). And these decreases had significant positive relations with the damaged phagocytosis of the aged Kupffer cell.gammavalues were 0.96(P < 0.05), 0.99(P < 0.01) and 0.95 (P < 0.05) respectively.CONCLUSION: The cytos-keleton system of the aged Kupffer cell presents an evident state of senescence, which may be an important mechanism of decreased phagocytosis of the aged Kupffer cell.
AIM:To investigate the mechanism of age-related reduction of Kupffer cell (KC) phagocytic capacity and the protective management.
METHODS:Using rhodamine 123 fluorescence density and rate of glucose utilization as parameters, we measured the mitochondrial energy metabolism status in vitro and the glucose utilization capacity of isolated rat liver Kupffer cells (KCs) from rats of various ages (6 mo, 12 mo, 18 mo and 24 mo) and the effect of vitamin E (VE) pretreatment (500 mg/kg/wk × 13 wk).
RESULTS:The rate of KC glucose utilization and the rhodamine fluorescence density of KC mitochondria of 18 mo-old untreated rats (NVEG) were significantly lower than that of 6 mo-old NVEG by 19.3% (4.0 nmol·h ± 0.4 nmol·h -1 10.6 cells -1 vs 5.7 nmol·h ± 0.6 nmol·h -1 10 6 cells -1 , P < 0.05) and 19.5% (80.5 ± 6.3 vs 100.0 ± 4.7, P < 0.01) respectively; Rate of KC glucose utilization and the rhodamine fluorescence density of KC mitochondria of 6 mo-old rats were also lower than the 24 mo-old NVEG by 35.1% (3.7 nmol·h ± 0.6 nmol·h , P < 0.01) and 32.1% (67.9 ± 7.4 vs 100.0 ± 4.7, P < 0.01) respectively.The two parameters of 18 mo-old VE pretreated rats (VEG) were significantly higher than those of 18 mo-old NVEG, and statistically comparable to those of 6 mo-old VEG. The two parameters of the 24 mo-old VEG were significantly higher in comparison with those of 24 mo-old NVEG, but still significantly lower than those of 6 mo-old
VEG.CONCLUSION: Aging has a significantly negative effect on KC energy metabolism, which can be alleviated by VE pretreatment. Sun WB, Ma RL, Peng ZM, Li K, Duan HC, Han BL. Protective effect of vitamin E on age-related alterations of Kupffer cell energy metabolism. World
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