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  • 1
    Online Resource
    Online Resource
    Altered Neuronal Activity Topography Markers in the Elderly with Increased Atherosclerosis
    Frontiers Media SA ; 2017
    In:  Frontiers in Aging Neuroscience Vol. 9 ( 2017-07-06)
    Details
    In: Frontiers in Aging Neuroscience, Frontiers Media SA, Vol. 9 ( 2017-07-06)
    Type of Medium: Online Resource
    ISSN: 1663-4365
    URL: Article
    DOI: 10.3389/fnagi.2017.00216
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2017
    detail.hit.zdb_id: 2558898-9
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  • 2
    Online Resource
    Online Resource
    Intestinal Ischemia-Reperfusion Suppresses Biliary Excretion of Hepatic Organic Anion Transporting Polypeptides Substrate
    Frontiers Media SA ; 2013
    In:  Journal of Pharmacy & Pharmaceutical Sciences Vol. 16, No. 5 ( 2013-12-17), p. 722-
    Details
    In: Journal of Pharmacy & Pharmaceutical Sciences, Frontiers Media SA, Vol. 16, No. 5 ( 2013-12-17), p. 722-
    Abstract: Purpose. Intestinal ischemia-reperfusion (I/R) causes gut dysfunction and promotes multi-organ failure. The liver and kidney can be affected by multi-organ failure after intestinal I/R. Organic anion transporting polypeptides (OATPs) and organic anion transporters (OATs) are recognized in a broad spectrum from endogenous compounds to xenobiotics, including clinically important drugs. Therefore, it is important for understanding the pharmacokinetics to obtain evidence of alterations in OATPs and OATs expression and transport activities. In the present study, we investigated the expression of rat Oatps and Oats after intestinal I/R. Methods. We used intestinal ischemia-reperfusion (I/R) model rats. Real-time PCR and Western blotting were used to assess mRNA and protein expression levels. Plasma concentration and biliary excretion of sulfobromophthalein (BSP), which is used as a model compound of organic anion drugs, were measured after intravenous administration in intestinal I/R rats. Results. Although Oat1 and Oat3 mRNA levels were not altered in the kidney, Oatp1a1, Oatp1b2 and Oatp2b1 mRNA levels in the liver were significantly decreased at 1-6 h after intestinal I/R. Moreover, Oatp1a1 and Oatp2b1 protein expression levels were decreased at 1 h after intestinal I/R. Plasma concentration of BSP, which is a typical substrate of Oatps, in intestinal I/R rats reperfused 1 h was increased than that in sham-operated rats. Moreover, the area under the concentration-time curve (AUC0-90) in intestinal I/R rats reperfused 1 h was significantly increased than that in sham-operated rats. The total clearance (CLtot) and the biliary clearance (CLbile) in intestinal I/R rats reperfused 1 h were significantly decreased than those in sham-operated rats. Conclusions. Oatp1a1 and Oatp2b1 expression levels are decreased by intestinal I/R. The decreases in these transporters cause alteration of pharmacokinetics of organic anion compound. The newly found influence of intestinal I/R on the expression and function of Oatps may be a key to perform appropriate drug therapy.This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page
    Type of Medium: Online Resource
    ISSN: 1482-1826 , 1482-1826
    URL: Article
    DOI: 10.18433/J3NC8P
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2013
    detail.hit.zdb_id: 1422972-9
    SSG: 15,3
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  • 3
    Online Resource
    Online Resource
    Intestinal P-glycoprotein Expression is Multimodally Regulated by Intestinal Ischemia-Reperfusion
    Frontiers Media SA ; 2014
    In:  Journal of Pharmacy & Pharmaceutical Sciences Vol. 17, No. 2 ( 2014-06-09), p. 266-
    Details
    In: Journal of Pharmacy & Pharmaceutical Sciences, Frontiers Media SA, Vol. 17, No. 2 ( 2014-06-09), p. 266-
    Abstract: Purpose. Reactive oxygen species (ROS) have multiple physiological effects that are amount-dependent. ROS are one of the causes of intestinal ischemia-reperfusion (I/R) injury. In this study, we investigated whether the amount of ROS and the degree of intestinal I/R injury affect the expression level of P-glycoprotein (P-gp). Methods. We used hydrogen peroxide (H2O2) as ROS in in vitro experiments. Intestinal I/R model rats, which were subjected 15-min ischemia (I/R-15), were used in in vivo experiments. Results. P-gp expression in Caco-2 cells was increased in response to 1 µM of H2O2 but decreased upon exposure to 10 mM of H2O2. We previously reported that P-gp expression is decreased after intestinal I/R with 30-min ischemia (I/R-30), which time a large amount of ROS is generated. I/R-15 induced slightly less mucosal and oxidative injury than did I/R-30. P-gp expression in the jejunum was increased at 1 h after I/R-15, and ileal paracellular permeability was increased. The blood concentration of tacrolimus, a P-gp substrate, was lower during 0-20 min but was higher during 40-90 min post-administration compared with that in the sham-operated rats. P-gp expression in the ileum was decreased at 6 h after I/R-15, due to abnormal localization of P-gp, resulting in a high blood tacrolimus concentration in rats reperfused for 6 h. Conclusions. ROS multimodally regulate P-gp expression depending on its amount. This is important for understanding the pattern of P-gp expression after intestinal I/R. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.
    Type of Medium: Online Resource
    ISSN: 1482-1826 , 1482-1826
    URL: Article
    DOI: 10.18433/J3JG7D
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2014
    detail.hit.zdb_id: 1422972-9
    SSG: 15,3
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  • 4
    Online Resource
    Online Resource
    The Decrease in Farnesoid X Receptor, Pregnane X Receptor and Constitutive Androstane Receptor in the Liver after Intestinal Ischemia-Reperfusion
    Frontiers Media SA ; 2012
    In:  Journal of Pharmacy & Pharmaceutical Sciences Vol. 15, No. 5 ( 2012-11-28), p. 616-
    Details
    In: Journal of Pharmacy & Pharmaceutical Sciences, Frontiers Media SA, Vol. 15, No. 5 ( 2012-11-28), p. 616-
    Abstract: Purpose. Intestinal ischemia-reperfusion (I/R) damages remote organs, including the liver, and promotes multi-organ failure (MOF). However, the molecular mechanisms underlying acute liver injury after intestinal I/R have not been completely elucidated. Farnesoid X receptor (FXR), pregnane X receptor (PXR) and constitutive androstane receptor (CAR) regulate metabolizing enzymes and transporters, and coordinately prevent hepatotoxicity reflecting an inability of appropriate excretion of endogenous toxic compounds. In this study, we assessed FXR, PXR and CAR expression levels and their localization levels in nuclei in the liver after intestinal I/R. We also investigated the effect of IL-6 on FXR, PXR and CAR expression levels and their localization levels in nuclei in in vitro experiments. Methods. We used intestinal I/R model rats. Moreover, HepG2 cells were used in in vitro study. Real-time PCR and Western blotting were used to assess mRNA and protein expression levels. Nuclear receptor localization in nuclei was analyzed by Western blotting using nuclear extracts. Results. FXR and PXR expression levels began to be decreased at 3 h, and FXR, PXR and CAR expression levels were decreased at 6 h after intestinal I/R. The localization levels of FXR, PXR and CAR in nuclei began to be decreased at 3 h, and all of them were decreased at 6 h after intestinal I/R. In HepG2 cells, FXR, PXR and CAR expression levels were decreased by 0.5-1 ng/mL, 0.5-100 ng/mL and 100 ng/mL IL-6 treatment for 24 h, respectively. FXR, PXR and CAR localization levels in nuclei were suppressed by 0.5-10 ng/mL, 10-100 ng/mL and 10-100 ng/mL IL-6 treatment for 24 h, respectively. Conclusions. FXR, PXR and CAR expression levels are decreased in the liver after intestinal I/R. IL-6 is one of main causes the decreases in expressions of these receptors. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.
    Type of Medium: Online Resource
    ISSN: 1482-1826 , 1482-1826
    URL: Article
    DOI: 10.18433/J38C88
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2012
    detail.hit.zdb_id: 1422972-9
    SSG: 15,3
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  • 5
    Online Resource
    Online Resource
    Intestinal Ischemia-Reperfusion Increases Efflux for Uric Acid Via Paracellular Route in the Intestine, but Decreases that Via Transcellular Route Mediated by BCRP
    Frontiers Media SA ; 2012
    In:  Journal of Pharmacy & Pharmaceutical Sciences Vol. 15, No. 2 ( 2012-04-26), p. 295-
    Details
    In: Journal of Pharmacy & Pharmaceutical Sciences, Frontiers Media SA, Vol. 15, No. 2 ( 2012-04-26), p. 295-
    Abstract: Purpose. Uric acid is thought to be one of the most important antioxidants in human biological fluids. Intestinal ischemia-reperfusion (I/R) is an important factor associated with high rates of morbidity and mortality. Reactive oxygen species (ROS) are responsible for intestinal I/R injury. The aim of this study was to clarify the efflux for uric acid from the intestine after intestinal I/R. Methods. We used intestinal ischemia-reperfusion (I/R) model rats. Serosal to mucosal flux for [14C]-uric acid was assessed by using Ussing-type diffusion chambers. BCRP/Bcrp expression was assessed by Western blot analysis. Caco-2 cells were used for a model of the intestinal epithelium, and rotenone was used as a mitochondrial dysfunction inducer. Results. Serosal to mucosal flux for uric acid was increased after intestinal I/R, and that for mannitol was also increased. Ko143, which is a BCRP inhibitor, did not affect the uric acid transport. The decreasing uric acid transport mediated by Bcrp was caused by decrease in the level of Bcrp homodimer, bridged by an S-S bond. The suppression of Bcrp S-S bond formation was associated with mitochondrial dysfunction. Moreover, BCRP S-S bond formation activity was decreased by rotenone in Caco-2 cells. Conclusions. Serosal to mucosal flux for uric acid is significantly increased via the paracelluler route, but that via the transcellular route mediated by Bcrp is decreased after intestinal I/R. The decreasing uric acid flux mediated by Bcrp is caused by suppression of Bcrp S-S bond formation. This suppression of Bcrp S-S bond formation may be related to mitochondrial dysfunction. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.
    Type of Medium: Online Resource
    ISSN: 1482-1826 , 1482-1826
    URL: Article
    DOI: 10.18433/J3W896
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2012
    detail.hit.zdb_id: 1422972-9
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  • 6
    Online Resource
    Online Resource
    Development of a novel bioresorbable bone substitute with a unidirectional porous structure
    Frontiers Media SA ; 2016
    In:  Frontiers in Bioengineering and Biotechnology Vol. 4 ( 2016)
    Details
    In: Frontiers in Bioengineering and Biotechnology, Frontiers Media SA, Vol. 4 ( 2016)
    Type of Medium: Online Resource
    ISSN: 2296-4185
    URL: Article
    DOI: 10.3389/conf.FBIOE.2016.01.01794
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2016
    detail.hit.zdb_id: 2719493-0
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