Attenuation of pro-inflammatory cytokines and oxidative stress by misoprostol in renal ischemia/reperfusion in rats

I. Cura-Esquivel, E. N. Delgado-Chávez, J. H. García-Narro, L. Torres-González, G. Alarcón-Galván, D. P. Moreno-Peña, D. E. Squivel-Figueroa, D. V. Cantú-Machuca, L. E. Muñoz-Espinosa, L. Garza-Ocañas, P. Cordero-Pérez

Research output: Contribution to journalArticle

Abstract

© 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.
Original languageEnglish
Pages (from-to)537-540
Number of pages4
JournalPharmazie
Volume73
Issue number9
DOIs
Publication statusPublished - 1 Jan 2018

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Misoprostol
Reperfusion
Oxidative Stress
Ischemia
Cytokines
Kidney
Necrosis
Synthetic Prostaglandins
Alprostadil
Metabolic Networks and Pathways
Acute Kidney Injury
Wistar Rats
Reactive Oxygen Species
Antioxidants

All Science Journal Classification (ASJC) codes

  • Pharmaceutical Science

Cite this

Cura-Esquivel, I., Delgado-Chávez, E. N., García-Narro, J. H., Torres-González, L., Alarcón-Galván, G., Moreno-Peña, D. P., ... Cordero-Pérez, P. (2018). Attenuation of pro-inflammatory cytokines and oxidative stress by misoprostol in renal ischemia/reperfusion in rats. Pharmazie, 73(9), 537-540. https://doi.org/10.1691/ph.2018/8498, https://doi.org/10.1691/ph.2018/8498
Cura-Esquivel, I. ; Delgado-Chávez, E. N. ; García-Narro, J. H. ; Torres-González, L. ; Alarcón-Galván, G. ; Moreno-Peña, D. P. ; Squivel-Figueroa, D. E. ; Cantú-Machuca, D. V. ; Muñoz-Espinosa, L. E. ; Garza-Ocañas, L. ; Cordero-Pérez, P. / Attenuation of pro-inflammatory cytokines and oxidative stress by misoprostol in renal ischemia/reperfusion in rats. In: Pharmazie. 2018 ; Vol. 73, No. 9. pp. 537-540.
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Cura-Esquivel, I, Delgado-Chávez, EN, García-Narro, JH, Torres-González, L, Alarcón-Galván, G, Moreno-Peña, DP, Squivel-Figueroa, DE, Cantú-Machuca, DV, Muñoz-Espinosa, LE, Garza-Ocañas, L & Cordero-Pérez, P 2018, 'Attenuation of pro-inflammatory cytokines and oxidative stress by misoprostol in renal ischemia/reperfusion in rats', Pharmazie, vol. 73, no. 9, pp. 537-540. https://doi.org/10.1691/ph.2018/8498, https://doi.org/10.1691/ph.2018/8498

Attenuation of pro-inflammatory cytokines and oxidative stress by misoprostol in renal ischemia/reperfusion in rats. / Cura-Esquivel, I.; Delgado-Chávez, E. N.; García-Narro, J. H.; Torres-González, L.; Alarcón-Galván, G.; Moreno-Peña, D. P.; Squivel-Figueroa, D. E.; Cantú-Machuca, D. V.; Muñoz-Espinosa, L. E.; Garza-Ocañas, L.; Cordero-Pérez, P.

In: Pharmazie, Vol. 73, No. 9, 01.01.2018, p. 537-540.

Research output: Contribution to journalArticle

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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.

PY - 2018/1/1

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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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