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- Hammes, T. O., et al.
(författare)
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Lactobacillus rhamnosus GG reduces hepatic fibrosis in a model of chronic liver disease in rats
- 2017
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Ingår i: Nutricion Hospitalaria. - : ARAN Ediciones. - 0212-1611 .- 1699-5198. ; 34:3, s. 702-709
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Tidskriftsartikel (refereegranskat)abstract
- Background: The intestinal dysbiosis is common in chronic liver disease and can induce to inflammatory responses and mediate the collagen deposition in the liver. Aim: To evaluate the probiotic Lactobacillus rhamnosus GG (LGG) for the treatment of liver fibrosis in a model of chronic cholestatic liver disease in rats. Methods: Male adult Wistar rats (n = 29) were submitted to common bile duct ligation (BDL groups) or manipulation of common bile duct without ligation (Ctrl groups).Two weeks after surgery, each group was randomly divided to receive 1 ml of PBS (Ctrl and BDL) or PBS containing 2.5 x 10(7) CFU of LGG (Ctrl-P and BDL-P) through gavages for 14 days. Euthanasia occurred 33 days after surgery when samples of blood and liver tissue were collected. Results: The hepatic gene expression of Tlr4, Tnf alpha, IL-6, Tgf beta, and metalloproteinase-2 and -9 were higher in the BDL groups in comparison to Ctrl. The ductular reaction evaluated by immunocontent of cytokeratin-7 (CK7) and the content of collagen were increased in BDL groups. Also, there was an imbalance in the antioxidant defenses (superoxide dismutase and catalase) and an increase in the oxidative stress marker sulfhydryl in BDL groups. The treatment with LGG significantly reduced gene expression of IL-6, collagen deposition, and ductular reaction in hepatic tissue of animals from BDL-P groups. Conclusion: The treatment with the probiotic LGG was able to reduce liver fibrosis, ductular reaction, and hepatic gene expression of IL-6 in a model of cholestatic liver disease in rats.
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| 2. |
- Leke, Renata, 1979, et al.
(författare)
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The glutamine transporters and their role in the glutamate/GABA-glutamine cycle
- 2016
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Ingår i: The Glutamate/GABA-Glutamine Cycle. - Cham : Springer. - 2190-5215. - 9783319450940 ; , s. 223-257
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Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
- Glutamine is a key amino acid in the CNS, playing an important role in the glutamate/GABA-glutamine cycle (GGC). In the GGC, glutamine is transferred from astrocytes to neurons, where it will replenish the inhibitory and excitatory neurotransmitter pools. Different transporters participate in this neural communication, i.e., the transporters responsible for glutamine efflux from astrocytes and influx into the neurons, such as the members of the SNAT, LAT, y+LAT, and ASC families of transporters. The SNAT family consists of the transporter isoforms SNAT3 and SNAT5 that are related to efflux from the astrocytic compartment, and SNAT1 and SNAT2 that are associated with glutamine uptake into the neuronal compartment. The isoforms SNAT7 and SNAT8 do not have their role completely understood, but they likely also participate in the GGC. The isoforms LAT2 and y+LAT2 facilitate the exchange of neutral amino acids and cationic amino acids (y+LAT2 isoform) and have been associated with glutamine efflux from astrocytes. ASCT2 is a Na+-dependent antiporter, the participation of which in the GGC also remains to be better characterized. All these isoforms are tightly regulated by transcriptional and translational mechanisms, which are induced by several determinants such as amino acid deprivation, hormones, pH, and the activity of different signaling pathways. Dysfunctional glutamine transporter activity has been associated with the pathophysiological mechanisms of certain neurologic diseases, such as Hepatic Encephalopathy and Manganism. However, there might also be other neuropathological conditions associated with an altered GGC, in which glutamine transporters are dysfunctional. Hence, it appears to be of critical importance that the physiological and pathological aspects of glutamine transporters are thoroughly investigated. © Springer International Publishing Switzerland 2016.
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| 3. |
- Wilhelmsson, Ulrika, 1970, et al.
(författare)
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Nestin Regulates Neurogenesis in Mice Through Notch Signaling From Astrocytes to Neural Stem Cells
- 2019
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Ingår i: Cerebral Cortex. - : Oxford University Press (OUP). - 1047-3211 .- 1460-2199. ; 29:10, s. 4050-4066
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Tidskriftsartikel (refereegranskat)abstract
- The intermediate filament (nanofilament) protein nestin is a marker of neural stem cells, but its role in neurogenesis, including adult neurogenesis, remains unclear. Here, we investigated the role of nestin in neurogenesis in adult nestin-deficient (Nes(-/-)) mice. We found that the proliferation of Nes(-/-) neural stem cells was not altered, but neurogenesis in the hippocampal dentate gyrus of Nes(-/-) mice was increased. Surprisingly, the proneurogenic effect of nestin deficiency was mediated by its function in the astrocyte niche. Through its role in Notch signaling from astrocytes to neural stem cells, nestin negatively regulates neuronal differentiation and survival; however, its expression in neural stem cells is not required for normal neurogenesis. In behavioral studies, nestin deficiency in mice did not affect associative learning but was associated with impaired long-term memory.
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