alexa Bupropion Cannot Reduce Acute Kidney Injury Due to Isch
ISSN: 2161-1459

Journal of Clinical & Experimental Pharmacology
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Research Article

Bupropion Cannot Reduce Acute Kidney Injury Due to Ischemia-Reperfusion

Guzmán-de la Garza FJ1,2*, Cabello-García AJ1, Ibarra-Hernandez JM2, Martini-Antonio MT1, Alarcón-Galván G3, Cámara-Lemaroy CR3, Vargas-Villarreal J1, Hernández SG1, Garza JC1, Muzquiz-Vidales R2, Cordero-Perez P3, Garza NEF2 and Salinas-Martinez AM1

1Mexican Institute of Social Security, Center for Biomedical Research of the Northeast, C.P. 64720, Mexico

2Department of Physiology, Universidad Autonoma de Nuevo Leon, C.P. 64460, Mexico

3Universidad Autonoma de Nuevo Leon, University Hospital "Dr. José Eleuterio González", C.P. 64460, Mexico

*Corresponding Author:
Guzmán-de la Garza FJ
Center for Biomedical Research in the Northeast
IMSS Street: 2 de Abril # 501 Esq., San Luis Potosi
Colonia: Independencia, Monterrey Nuevo León, 64720, Mexico
Tel: +52 8112081921
E-mail: [email protected]

Received date: April 21, 2017; Accepted date: May 17, 2017; Published date: May 22, 2017

Citation: Guzmán-de la Garza FJ, Cabello-García AJ, Ibarra-Hernandez JM, Martini-Antonio MT, Alarcón-Galván G, et al. (2017) Bupropion Cannot Reduce Acute Kidney Injury Due to Ischemia-Reperfusion. Clin Exp Pharmacol 7:239. doi: 10.4172/2161-1459.1000239

Copyright: © 2017 Guzmán-de la Garza FJ, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Bupropion can limit the increase of TNF-alpha, reducing the inflammatory response and injury due to Ischemia- Reperfusion (I/R) on tissues such as the bowel. Our objective was to evaluate bupropion as a preconditioning agent for ischemic acute kidney injury.

Experiments were performed on female Wistar rats. Bupropion groups received 25 mg/kg 60 min before the maneuver. As a first step, 30 rats with a right nephrectomy were divided into 6 groups (n=5): sham 24, sham 48, bupropion 24, bupropion 48, ischemia-reperfusion 24 and ischemia-reperfusion 48. After 60 min of ischemia (except sham groups) 24 or 48 h of reperfusion was allowed. During a second step, 30 rats, with both kidneys conserved, were divided into 6 groups (n=5): sham 3, sham 72, bupropion 3, bupropion 72, ischemia-reperfusion 3, and ischemia-reperfusion 72 (IR72). Ischemia in these groups (except sham groups) was performed for 60 min only on the left kidney, and 3 or 72 h of reperfusion were allowed. Serum and histologic evaluations were done.

After 48 h of reperfusion, all mono-renal rats that received bupropion died. Bupropion cannot avoid histological damage nor does it impact creatinine clearance, BUN, TNF-α or KIM-1 serum levels secondary to I/R. In conclusion: The pharmacologic preconditioning with Bupropion cannot improve the AKI evolution in rats with renal ischemiareperfusion injury.

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