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  • Standardized extract of Bacopa monniera (BESEB CDRI-08) attenuates contextual associative learning deficits in the aging rat's brain induced by D-galactose. 22715050

    In this study, we examined the neuroprotective effect of standardized Bacopa monniera extract (BME: BESEB CDRI-08) against the D-galactose (D-gal)-induced brain aging in rats. Experimental groups were subjected to contextual-associative learning task. We found that the administration of BME in the D-gal-treated group attenuated contextual-associative learning deficits; the individuals showed more correct responses and retrieved the reward with less latency. Subsequent analysis showed that the BME administration significantly decreased advance glycation end product (AGE) in serum and increased the activity of antioxidant response element (ARE) and the antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and nuclear transcription factor NF-E2-related factor 2 (Nrf2), accompanied by a reduction in the level of serotonin (5-HT) in the hippocampus. The BME treatment also reversed D-gal-induced brain aging by upregulating the levels of the presynaptic proteins synaptotagmin I (SYT1) and synaptophysin (SYP) and the postsynaptic proteins Ca(2+) /calmodulin dependent protein kinase II (αCaMKII) and postsynaptic density protein-95 (PSD-95) in the hippocampus during synaptic plasticity. A significant finding is that the D-gal- + BME-treated rats exhibited more correct responses in contextual-associative learning than D-gal alone-treated rats. Our findings suggest that BME treatment attenuates D-gal-induced brain aging and regulates the level of antioxidant enzymes, Nrf2 expression, and the level of 5-HT, which was accompanied by concomitantly increased levels of synaptic proteins SYT1, SYP, αCaMKII, p-αCaMKII, and PSD-95. © 2012 Wiley Periodicals, Inc.
    Document Type:
    Reference
    Product Catalog Number:
    04-1019

  • Effects of oral fat perception by modified sham feeding on energy expenditure, hormones and appetite profile in the postprandial state. 18814804

    Previously, we have shown that satiety and metabolites increased after high-fat modified sham feeding (MSF). We assessed possible metabolic effects due to oral stimulation with a high-fat sham-fed 'meal', in comparison with a high-fat fed meal and with water, in the postprandial state. Fourteen healthy women (aged 18-40 years; BMI 22.5 (SD 3) kg/m2) were fed in energy balance during 4 d with a 50 % energy as carbohydrate, 15 % energy as protein and 35 % energy as fat menu. On day 4, subjects were given one out of three test lunches, 5 h after a high-fat breakfast, in random order: a high-fat MSF lunch, water (W) or the same lunch to be eaten (E), during their 36 h stay in the respiration chamber, where substrate oxidation, 24 h energy expenditure (EE) and appetite profile were measured. Oral fat stimulation by MSF increased EE (W 6.3 (SD 0.8) v. MSF 6.9 (SD 1.0) kJ/min and E 6.8 (SD 0.7) kJ/min; P < 0.04) for 1 h, increased plasma insulin concentrations (t = 15; W 10.0 (SD 3.4) v. MSF 13.2 (SD 4.0) v. E 22.3 (SD 3.3) units/l; P < 0.0001), attenuated changes in plasma NEFA concentrations (t = 15, W 432 (SD 108) v. MSF 418 (SD 146) v. E 282 (SD 72) micromol/l; P < 0.0001), plasma TAG concentrations (t = 60; W 1092 (SD 548) v. MSF 1116 (SD 493) micromol/l and E 1350 (SD 352) micromol/l; P < 0.02) and plasma glycerol concentrations (t = 15, W 87 (SD 29) v. MSF 74 (SD 34) micromol/l and E 67 (SD 18) micromol/l; P < 0.03). Over a longer period of time, MSF had no effects on substrate oxidation, diet-induced thermogenesis or total EE. In addition to the previously observed metabolic effects of oral stimulation with fat, EE is stimulated up to 1 h after the MSF meal.
    Document Type:
    Reference
    Product Catalog Number:
    EGLP-35K
    Product Catalog Name:
    Glucagon Like Peptide-1 (Active) ELISA

  • Impact of endurance training on murine spontaneous activity, muscle mitochondrial DNA abundance, gene transcripts, and function. 17110513

    We hypothesized that enhanced skeletal muscle mitochondrial function following aerobic exercise training is related to an increase in mitochondrial transcription factors, DNA abundance [mitochondrial DNA (mtDNA)], and mitochondria-related gene transcript levels, as well as spontaneous physical activity (SPA) levels. We report the effects of daily treadmill training on 12-wk-old FVB mice for 5 days/wk over 8 wk at 80% peak O(2) consumption and studied the training effect on changes in body composition, glucose tolerance, muscle mtDNA muscle, mitochondria-related gene transcripts, in vitro muscle mitochondrial ATP production capacity (MATPC), and SPA levels. Compared with the untrained mice, the trained mice had higher peak O(2) consumption (+18%; P < 0.001), lower percentage of abdominal (-25.4%; P < 0.02) and body fat (-19.5%; P < 0.01), improved glucose tolerance (P < 0.04), and higher muscle mitochondrial enzyme activity (+19.5-43.8%; P < 0.04) and MATPC (+28.9 to +32.4%; P < 0.01). Gene array analysis showed significant differences in mRNAs of mitochondria-related ontology groups between the trained and untrained mice. Training also increased muscle mtDNA (+88.4 to +110%; P < 0.05), peroxisome proliferative-activated receptor-gamma coactivator-1alpha protein (+99.5%; P < 0.04), and mitochondrial transcription factor A mRNA levels (+21.7%; P < 0.004) levels. SPA levels were higher in trained mice (P = 0.056, two-sided t-test) and significantly correlated with two separate substrate-based measurements of MATPC (P < 0.02). In conclusion, aerobic exercise training enhances muscle mitochondrial transcription factors, mtDNA abundance, mitochondria-related gene transcript levels, and mitochondrial function, and this enhancement in mitochondrial function occurs in association with increased SPA.
    Document Type:
    Reference
    Product Catalog Number:
    EZRMI-13K
    Product Catalog Name:
    Rat/Mouse Insulin ELISA

  • Upregulation of the E3 ligase NEDD4-1 by oxidative stress degrades IGF-1 receptor protein in neurodegeneration. 22875931

    The importance of ubiquitin E3 ligases in neurodegeneration is being increasingly recognized. The crucial role of NEDD4-1 in neural development is well appreciated; however, its role in neurodegeneration remains unexplored. Herein, we report increased NEDD4-1 expression in the degenerated tissues of several major neurodegenerative diseases. Moreover, its expression is upregulated in cultured neurons in response to various neurotoxins, including zinc and hydrogen superoxide, via transcriptional activation likely mediated by the reactive oxygen species (ROS)-responsive FOXM1B. Reduced protein levels of the insulin-like growth factor receptor (IGF-1Rβ) were observed as a consequence of upregulated NEDD4-1 via the ubiquitin-proteasome system. Overexpression of a familial mutant form of superoxide dismutase 1 (SOD1) (G93A) in neuroblastoma cells resulted in a similar reduction of IGF-1Rβ protein. This inverse correlation between NEDD4-1 and IGF-1Rβ was also observed in the cortex and spinal cords of mutant (G93A) SOD1 transgenic mice at a presymptomatic age, which was similarly induced by in vivo-administered zinc in wild-type C57BL/6 mice. Furthermore, histochemistry reveals markedly increased NEDD4-1 immunoreactivity in the degenerating/degenerated motor neurons in the lumbar anterior horn of the spinal cord, suggesting a direct causative role for NEDD4-1 in neurodegeneration. Indeed, downregulation of NEDD4-1 by shRNA or overexpression of a catalytically inactive form rescued neurons from zinc-induced cell death. Similarly, neurons with a NEDD4-1 haplotype are more resistant to apoptosis, largely due to expression of higher levels of IGF-1Rβ.Together, our work identifies a novel molecular mechanism for ROS-upregulated NEDD4-1 and the subsequently reduced IGF-1Rβ signaling in neurodegeneration.
    Document Type:
    Reference
    Product Catalog Number:
    07-049
    Product Catalog Name:
    Anti-Nedd4

  • Myoblast-seeded biodegradable scaffolds to prevent post-myocardial infarction evolution toward heart failure. 16798312

    OBJECTIVE(S): Even though the mechanism is not clearly understood, direct intramyocardial cell transplantation has demonstrated potential to treat patients with severe heart failure. We previously reported on the bioengineering of myoblast-based constructs. We investigate here the functional outcome of infarcted hearts treated by implantation of myoblast-seeded scaffolds. METHODS: Adult Lewis rats with echocardiography-confirmed postinfarction reduced ejection fraction (48.3% +/- 1.1%) were randomized to (1) implantation of myoblast-seeded polyurethane patches at the site of infarction (PU-MyoB, n = 11), (2) implantation of nonseeded polyurethane patches (PU, n = 11), (3) sham operation (Sham, n = 12), and (4) direct intramyocardial myoblast injection (MyoB, n = 11). Four weeks later, the functional assessment by echocardiography was repeated, and we additionally performed left ventricular catheterization plus histologic studies. RESULTS: The ejection fraction significantly decreased in the PU (39.1% +/- 2.3%; P = .02) and Sham (39.9% +/- 3.5%; P = .04) groups, whereas it remained stable in the PU-MyoB (48.4% +/- 3.1%) and MyoB (47.9% +/- 3.0%) groups during the observation time. Similarly, left ventricular contractility was significantly higher in groups PU-MyoB (4960 +/- 266 mm Hg/s) and MyoB (4748 +/- 304 mm Hg/s) than in groups PU (3909 +/- 248 mm Hg/s, P = .01) and Sham (4028 +/- 199 mm Hg/s, P = .01). Immunohistology identified a high density of myoblasts within the seeded scaffolds without any migration toward the host cardiac tissue and no evidence of cardiac cell differentiation. CONCLUSIONS: Myoblast-seeded polyurethane scaffolds prevent post-myocardial infarction progression toward heart failure as efficiently as direct intramyocardial injection. The immunohistologic analysis suggests that an indirect mechanism, potentially a paracrine effect, may be assumed.
    Document Type:
    Reference
    Product Catalog Number:
    MAB1628
    Product Catalog Name:
    Anti-Myosin Antibody, slow muscle, clone NOQ7.5.4D

  • A small-molecule inhibitor of Haspin alters the kinetochore functions of Aurora B. 23071153

    By phosphorylating Thr3 of histone H3, Haspin promotes centromeric recruitment of the chromosome passenger complex (CPC) during mitosis. Aurora B kinase, a CPC subunit, sustains chromosome bi-orientation and the spindle assembly checkpoint (SAC). Here, we characterize the small molecule 5-iodotubercidin (5-ITu) as a potent Haspin inhibitor. In vitro, 5-ITu potently inhibited Haspin but not Aurora B. Consistently, 5-ITu counteracted the centromeric localization of the CPC without affecting the bulk of Aurora B activity in HeLa cells. Mislocalization of Aurora B correlated with dephosphorylation of CENP-A and Hec1 and SAC override at high nocodazole concentrations. 5-ITu also impaired kinetochore recruitment of Bub1 and BubR1 kinases, and this effect was reversed by concomitant inhibition of phosphatase activity. Forcing localization of Aurora B to centromeres in 5-ITu also restored Bub1 and BubR1 localization but failed to rescue the SAC override. This result suggests that a target of 5-ITu, possibly Haspin itself, may further contribute to SAC signaling downstream of Aurora B.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • n-Pentane (Éire)

    Document Type:
    SDS
    Product Catalog Number:
    109719
    Product Catalog Name:
    n-Pentane