TY - JOUR
T1 - Attenuation of pro-inflammatory cytokines and oxidative stress by misoprostol in renal ischemia/reperfusion in rats
AU - Cura-Esquivel, I.
AU - Delgado-Chávez, E. N.
AU - García-Narro, J. H.
AU - Torres-González, L.
AU - Alarcón-Galván, G.
AU - Moreno-Peña, D. P.
AU - Squivel-Figueroa, D. E.
AU - Cantú-Machuca, D. V.
AU - Muñoz-Espinosa, L. E.
AU - Garza-Ocañas, L.
AU - Cordero-Pérez, P.
N1 - Publisher Copyright:
© 2018 Govi-Verlag Pharmazeutischer Verlag GmbH. All rights reserved.
PY - 2018/1/1
Y1 - 2018/1/1
N2 - © 2018 Govi-Verlag Pharmazeutischer Verlag GmbH. All rights reserved. The ischemia/reperfusion (I/R) process alters metabolic pathways, releasing reactive oxygen species and pro-inflammatory cytokines that cause tissue necrosis and activate cellular apoptotic pathways. Misoprostol (MSP) is a prostaglandin E1 analog that has demonstrated a cytoprotective role in the I/R process. The study objective was to evaluate the effects of MSP on the regulation of pro-inflammatory and oxidative stress mediators in an I/R-induced acute kidney injury rat model. Wistar rats were divided into 3 groups. Sham and I/R were given 1 mL/day of physiological solution; MSP+I/R was given intragastric MSP (300 μg/kg) for 3 days. For I/R and MSP+IR, the renal hilum was clamped for 45 min, followed by 15 h of reperfusion. Renal function tests, pro-inflammatory cytokines, mediators of oxidative stress, and histological analysis were evaluated. Pro-inflammatory cytokine activity was significantly attenuated in the MSP+I/R group. However, there was no statistically significant difference between Sham and MSP. Regarding antioxidant activity, MSP+I/R showed a significant decrease in these mediators compared with Sham and I/R. Histologically, scarce medullary necrosis was observed with a preserved renal cortex in the MSP group.
AB - © 2018 Govi-Verlag Pharmazeutischer Verlag GmbH. All rights reserved. The ischemia/reperfusion (I/R) process alters metabolic pathways, releasing reactive oxygen species and pro-inflammatory cytokines that cause tissue necrosis and activate cellular apoptotic pathways. Misoprostol (MSP) is a prostaglandin E1 analog that has demonstrated a cytoprotective role in the I/R process. The study objective was to evaluate the effects of MSP on the regulation of pro-inflammatory and oxidative stress mediators in an I/R-induced acute kidney injury rat model. Wistar rats were divided into 3 groups. Sham and I/R were given 1 mL/day of physiological solution; MSP+I/R was given intragastric MSP (300 μg/kg) for 3 days. For I/R and MSP+IR, the renal hilum was clamped for 45 min, followed by 15 h of reperfusion. Renal function tests, pro-inflammatory cytokines, mediators of oxidative stress, and histological analysis were evaluated. Pro-inflammatory cytokine activity was significantly attenuated in the MSP+I/R group. However, there was no statistically significant difference between Sham and MSP. Regarding antioxidant activity, MSP+I/R showed a significant decrease in these mediators compared with Sham and I/R. Histologically, scarce medullary necrosis was observed with a preserved renal cortex in the MSP group.
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U2 - 10.1691/ph.2018/8498
DO - 10.1691/ph.2018/8498
M3 - Article
AN - SCOPUS:85053785372
SN - 0031-7144
VL - 73
SP - 537
EP - 540
JO - Pharmazie
JF - Pharmazie
IS - 9
ER -