3-(6-isobutyl-9-methoxy-1-4-dioxo-1-2-3-4-6-7-12-12a-octahydropyrazino(1--2--1-6)pyrido(3-4-b)indol-3-yl)propionic-acid-tert-butyl-ester and Reperfusion-Injury

3-(6-isobutyl-9-methoxy-1-4-dioxo-1-2-3-4-6-7-12-12a-octahydropyrazino(1--2--1-6)pyrido(3-4-b)indol-3-yl)propionic-acid-tert-butyl-ester has been researched along with Reperfusion-Injury* in 1 studies

Other Studies

1 other study(ies) available for 3-(6-isobutyl-9-methoxy-1-4-dioxo-1-2-3-4-6-7-12-12a-octahydropyrazino(1--2--1-6)pyrido(3-4-b)indol-3-yl)propionic-acid-tert-butyl-ester and Reperfusion-Injury

Article	Year
Intestinal ischemia-reperfusion increases efflux for uric acid via paracellular route in the intestine, but decreases that via transcellular route mediated by BCRP. Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques, 2012, Volume: 15, Issue:2 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.. 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.. 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.. 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. Topics: Adenosine; Animals; ATP Binding Cassette Transporter, Subfamily G, Member 2; ATP-Binding Cassette Transporters; Caco-2 Cells; Cell Survival; Diketopiperazines; Heterocyclic Compounds, 4 or More Rings; Humans; Intestinal Mucosa; Intestines; Male; Mitochondria; Neoplasm Proteins; Rats; Rats, Wistar; Reperfusion Injury; Rotenone; Uncoupling Agents; Uric Acid	2012

Article

Year

Intestinal ischemia-reperfusion increases efflux for uric acid via paracellular route in the intestine, but decreases that via transcellular route mediated by BCRP.

Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques, 2012, Volume: 15, Issue:2

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.. 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.. 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.. 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.

Topics: Adenosine; Animals; ATP Binding Cassette Transporter, Subfamily G, Member 2; ATP-Binding Cassette Transporters; Caco-2 Cells; Cell Survival; Diketopiperazines; Heterocyclic Compounds, 4 or More Rings; Humans; Intestinal Mucosa; Intestines; Male; Mitochondria; Neoplasm Proteins; Rats; Rats, Wistar; Reperfusion Injury; Rotenone; Uncoupling Agents; Uric Acid

2012