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排序方式: 共有195条查询结果,搜索用时 31 毫秒
101.
Nicastro H Gualano B de Moraes WM de Salles Painelli V da Luz CR dos Santos Costa A de Salvi Guimarães F Medeiros A Brum PC Lancha AH 《Amino acids》2012,42(5):1695-1701
We aimed to investigate the possible role of creatine (CR) supplementation in counteracting dexamethasone-induced muscle wasting
and insulin resistance in rats. Also, we examined whether CR intake would modulate molecular pathways involved in muscle remodeling
and insulin signaling. Animals were randomly divided into four groups: (1) dexamethasone (DEX); (2) control pair-fed (CON-PF);
(3) dexamethasone plus CR (DEX-CR); and (4) CR pair-fed (CR-PF). Dexamethasone (5 mg/kg/day) and CR (5 g/kg/day) were given
via drinking water for 7 days. Plantaris and extensor digitorum longus (EDL) muscles were removed for analysis. Plantaris
and EDL muscle mass were significantly reduced in the DEX-CR and DEX groups when compared with the CON-PF and CR-PF groups
(P < 0.05). Dexamethasone significantly decreased phospho-Ser473-Akt protein levels compared to the CON-PF group (P < 0.05) and CR supplementation aggravated this response (P < 0.001). Serum glucose was significantly increased in the DEX group when compared with the CON-PF group (DEX 7.8 ± 0.6 vs.
CON-PF 5.2 ± 0.5 mmol/l; P < 0.05). CR supplementation significantly exacerbated hyperglycemia in the dexamethasone-treated animals (DEX-CR 15.1 ± 2.4 mmol/l;
P < 0.05 vs. others). Dexamethasone reduced GLUT-4 translocation when compared with the CON-PF and CR-PF (P < 0.05) groups and this response was aggravated by CR supplementation (P < 0.05 vs. others). In conclusion, supplementation with CR resulted in increased insulin resistance and did not attenuate
muscle wasting in rats treated with dexamethasone. Given the contrast with the results of human studies that have shown benefits
of CR supplementation on muscle atrophy and insulin sensitivity, we suggest caution when extrapolating this animal data to
human subjects. 相似文献
102.
AJ Teodoro FL Oliveira NB Martins GA Maia RB Martucci R Borojevic 《Cancer cell international》2012,12(1):36-9
ABSTRACT: BACKGROUND: Lycopene, a major carotenoid component of tomato, has a potential anticancer activity in many types of cancer. Epidemiological and clinical trials rarely provide evidence for mechanisms of the compound's action, and studies on its effect on cancer of different cell origins are now being done. The aim of the present study was to determine the effect of lycopene on cell cycle and cell viability in eight human cancer cell lines. METHODS: Human cell lines were treated with lycopene (1-5 uM) for 48 and 96 h. Cell viability was monitored using the method of MTT. The cell cycle was analyzed by flow cytometry, and apoptotic cells were identified by terminal deoxynucleotidyl transferase-mediated dUTP nick labeling (TUNEL) and by DAPI. RESULTS: Our data showed a significant decrease in the number of viable cells in three cancer cells lines (HT-29, T84 and MCF-7) after 48 h treatment with lycopene, and changes in the fraction of cells retained in different cell cycle phases. Lycopene promoted also cell cycle arrest followed by decreased cell viability in majority of cell lines after 96 h, as compared to controls. Furthermore, an increase in apoptosis was observed in four cell lines (T-84, HT-29, MCF-7 and DU145) when cells were treated with lycopene. CONCLUSIONS: Our findings show the capacity of lycopene to inhibit cell proliferation, arrest cell cycle in different phases and increase apoptosis, mainly in breast, colon and prostate lines after 96 h. These observations suggest that lycopene may alter cell cycle regulatory proteins depending on the type of cancer and the dose of lycopene administration. Taken together, these data indicated that the antiproliferative effect of lycopene was cellular type, time and dose-dependent. KEY WORDS: lycopene, cancer, bioactive compounds, cell cycle. 相似文献
103.
Angelo PC Ferreira AC Fonseca VD Frade SP Ferreira CS Malta FS Pereira AK Leite HV Brum AP Pardini VC Gomes KB Cabral AC 《Genetics and molecular research : GMR》2012,11(2):1002-1012
Cryopreservation of mesenchymal stem cells from amniotic fluid is of clinical importance, as these cells can be harvested during the prenatal period and stored for use in treatments. We examined the behavior of mesenchymal stem cells from human amniotic fluid in culture that had been subjected to cryopreservation. We assessed chromosomal stability through karyotype analysis, determined whether multipotent capacity (differentiation into adipogenic, chondrogenic, and osteogenic cells) is maintained, and analyzed SOX2 and NANOG expression after thawing. Five amniotic fluid samples were cryopreserved for 150 days. No chromosomal aberrations were observed. The expression levels of NANOG and SOX2 also were quite similar before and after cryopreservation. Capacity for differentiation into adipogenic, chondrogenic, and osteogenic tissues also remained the same. We conclude that cryopreservation of amniotic fluid does not alter karyotype, NANOG/SOX2 gene expression, or multipotent capacity of stem cells that have been collected from amniotic fluid during pregnancy. 相似文献
104.
Marilia Bianca Cruz Grecco Teixeira Gisele Miyamura Martins Manuela Miranda-Rodrigues Iasmin Ferreira De Araújo Ricardo Oliveira Patrícia Chakur Brum Cecilia Helena Azevedo Gouveia 《PloS one》2016,11(1)
A series of studies have demonstrated that activation of the sympathetic nervous system (SNS) causes osteopenia via β2-adrenoceptor (β2-AR) signaling. However, in a recent study, we found an unexpected and generalized phenotype of high bone mass in female mice with chronic sympathetic hyperactivity, due to double gene inactivation of adrenoceptors that negatively regulate norepinephrine release, α2A-and α2C-AR (α2A/2C-AR-/-). These findings suggest that β2-AR is not the single adrenoceptor involved in bone turnover regulation and show that α2-AR signaling may also mediate the SNS actions in the skeleton. In addition, we found that α2A/2C-AR-/- animals are resistant to the thyrotoxicosis-induced osteopenia, suggesting that thyroid hormone (TH), when in supraphysiological levels, interacts with the SNS to control bone mass and structure, and that this interaction may also involve α2-AR signaling. In the present study, to further investigate these hypotheses and to discriminate the roles of α2-AR subtypes, we have evaluated the bone phenotype of mice with the single gene inactivation of α2C-AR subtype, which mRNA expression was previously shown to be down regulated by triiodothyronine (T3). A cohort of 30 day-old female α2CAR-/- mice and their wild-type (WT) controls were treated with a supraphysiological dose of T3 for 30 or 90 days, which induced a thyrotoxic state in both mouse lineages. The micro-computed tomographic (μCT) analysis showed that α2C-AR-/- mice present lower trabecular bone volume (BV/TV) and number (Tb.N), and increased trabecular separation (Tb.Sp) in the femur compared with WT mice; which was accompanied by decreased bone strength (determined by the three-point bending test) in the femur and tibia. The opposite was observed in the vertebra, where α2C-AR-/- mice show increased BV/TV, Tb.N and trabecular thickness (Tb.Th), and decreased Tb.Sp, compared with WT animals. In spite of the contrasting bone phenotypes of the femur and L5, thyrotoxicosis negatively regulated most of the micro architectural features of the trabecular bone in both skeletal sites of WT, but not of α2C-AR-/- mice. T3 treatment also decreased biomechanical properties (maximum load and ultimate load) in the femur and tibia of WT, but not of knockout mice. The mRNA expression of osteocalcin, a marker of mature osteoblasts, and tartrate-resistant acid phosphatase, which is expressed by osteoclasts and is involved in collagen degradation, was increased by T3 treatment only in WT, and not in α2C-AR-/- mice. Altogether, these findings suggest that α2C-AR subtype mediates the effects of the SNS in the bone in a skeletal site-dependent manner, and that thyrotoxicosis depends on α2C-AR signaling to promote bone loss, which sustains the hypothesis of a TH-SNS interaction to modulate bone remodeling and structure. 相似文献
105.
106.
Heloísa D. Brum Henrique E. M. Nascimento William F. Laurance Ana C. S. Andrade Susan G. Laurance Regina C. C. Luizão 《Plant Ecology》2008,199(2):209-215
We summarize a long-term study of the effects of edge creation on establishment of the economically important arboreal palm
Oenocarpus bacaba in an experimentally fragmented landscape in central Amazonia. Recruitment and mortality of large individuals (≥10 cm diameter-at-breast-height) were recorded within 21 1-ha plots in fragmented
and intact forests for periods of up to 22 years. In addition, 12 small (0.7 × 14 m) sub-plots within each 1-ha plot were
used to enumerate the abundance of seedlings and saplings (5–400 cm tall). On average, the recruitment of large trees was
over two times faster near forest edges, leading to a sharp (90%) increase in the mean population density of large individuals
near forest edges, whereas the density of larger trees remained constant in the forest interior. Overall seedling and sapling
density was significantly lower in edge than interior plots, but edge plots had a much higher proportion of larger (>100 cm
tall) saplings. Our findings demonstrate that forest edges can have complex effects on tree demography and that one must consider
all tree life stages in order to effectively assess their effects on plant populations. 相似文献
107.
Differential effects of voltage-dependent inactivation and local anesthetics on kinetic phases of Ca2+ release in frog skeletal muscle
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In voltage-clamped frog skeletal muscle fibers, Ca(2+) release rises rapidly to a peak, then decays to a nearly steady state. The voltage dependence of the ratio of amplitudes of these two phases (p/s) shows a maximum at low voltages and declines with further depolarization. The peak phase has been attributed to a component of Ca(2+) release induced by Ca(2+), which is proportionally greater at low voltages. We compared the effects of two interventions that inhibit Ca(2+) release: inactivation of voltage sensors, and local anesthetics reputed to block Ca(2+) release induced by Ca(2+). Holding the cells partially depolarized strongly reduced the peak and steady levels of Ca(2+) release elicited by a test pulse and suppressed the maximum of the p/s ratio at low voltages. The p/s ratio increased monotonically with test voltage, eventually reaching a value similar to the maximum found in noninactivated fibers. This implies that the marked peak of Ca(2+) release is a property of a cooperating collection of voltage sensors rather than individual ones. Local anesthetics reduced the peak of release flux at every test voltage, and the steady phase to a lesser degree. At variance with sustained depolarization, they made p/s low at all voltages. These observations were well-reproduced by the "couplon" model of dual control, which assumes that depolarization and anesthetics respectively, and selectively, disable its Ca(2+)-dependent or its voltage-operated channels. This duality of effects and their simulation under such hypotheses are consistent with the operation of a dual, two-stage control of Ca(2+) release in muscle, whereby Ca(2+) released through multiple directly voltage-activated channels builds up at junctions to secondarily open Ca(2+)-operated channels. 相似文献
108.
109.
Felipe C. G. Reis Anderson S. Haro Aline V. N. Bacurau Sandro M. Hirabara Frederick Wasinski Milene S. Ormanji José B. N. Moreira Beatriz H. Kiyomoto Clelia R. A. Bertoncini Patricia C. Brum Rui Curi Michael Bader Reury F. P. Bacurau Jo?o B. Pesquero Ronaldo C. Araújo 《PloS one》2015,10(8)
Metabolic syndrome is a cluster of metabolic risk factors such as obesity, diabetes and cardiovascular diseases. Mitochondria is the main site of ATP production and its dysfunction leads to decreased oxidative phosphorylation, resulting in lipid accumulation and insulin resistance. Our group has demonstrated that kinins can modulate glucose and lipid metabolism as well as skeletal muscle mass. By using B2 receptor knockout mice (B2R-/-) we investigated whether kinin action affects weight gain and physical performance of the animals. Our results show that B2R-/- mice are resistant to high fat diet-induced obesity, have higher glucose tolerance as well as increased mitochondrial mass. These features are accompanied by higher energy expenditure and a lower feed efficiency associated with an increase in the proportion of type I fibers and intermediary fibers characterized by higher mitochondrial content and increased expression of genes related to oxidative metabolism. Additionally, the increased percentage of oxidative skeletal muscle fibers and mitochondrial apparatus in B2R-/- mice is coupled with a higher aerobic exercise performance. Taken together, our data give support to the involvement of kinins in skeletal muscle fiber type distribution and muscle metabolism, which ultimately protects against fat-induced obesity and improves aerobic exercise performance. 相似文献
110.
Yuansha Chen Peter Bystricky Jacob Adeyeye Pinaki Panigrahi Afsar Ali Judith A Johnson CA Bush JG MorrisJr OC Stine 《BMC microbiology》2007,7(1):20