Spironolactone Effect in Hepatic Ischemia/Reperfusion Injury in Wistar Rats

Julio César Jiménez Pérez, Araní Casillas Ramírez, Liliana Torres González, Linda Elsa Muñoz Espinosa, Marlene Marisol Perales Quintana, Gabriela Alarcón Galván, Homero Zapata Chavira, Francisco Javier Guzmán De La Garza, Carlos Rodrigo Cámara Lemarroy, Nancy Esthela Fernández Garza, Edelmiro Pérez Rodríguez, Paula Cordero Pérez

Resultado de la investigaciónrevisión exhaustiva

4 Citas (Scopus)


© 2016 Julio César Jiménez Pérez et al. Introduction. Ischemia/reperfusion (IR) injury, often associated with liver surgery, is an unresolved problem in the clinical practice. Spironolactone is an antagonist of aldosterone that has shown benefits over IR injury in several tissues, but its effects in hepatic IR are unknown. Objective. To evaluate the effect of spironolactone on IR-induced damage in liver. Materials and Methods. Total hepatic ischemia was induced in rats for 20 min followed by 60 min of reperfusion. Spironolactone was administered and hepatic injury, cytokine production, and oxidative stress were assessed. Results. After IR, increased transaminases levels and widespread acute inflammatory infiltrate, disorganization of hepatic hemorrhage trabeculae, and presence of apoptotic bodies were observed. Administration of SPI reduced biochemical and histological parameters of liver injury. SPI treatment increased IL-6 levels when compared with IR group but did not modify either IL-1β or TNF-α with respect to IR group. Regarding oxidative stress, increased levels of catalase activity were recorded in IR + SPI group in comparison with group without treatment, whereas MDA levels were similar in IR + SPI and IR groups. Conclusions. Spironolactone reduced the liver damage induced by IR, and this was associated with an increase in IL-6 production and catalase activity.
Idioma originalEnglish
PublicaciónOxidative Medicine and Cellular Longevity
EstadoPublished - 1 ene 2016
Publicado de forma externa

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Ageing
  • Cell Biology

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