Effect of Telmisartan in the Oxidative Stress Components Induced by Ischemia Reperfusion in Rats.

Simón Quetzalcoatl Rodríguez-Lara,Teresa Arcelia Garcia-Cobián,Alejandra Guillermina Miranda-Díaz,Ernesto Javier Ramírez-Lizardo,Ernesto German Cardona-Muñoz,Leonel García-Benavides,Walter Angel Trujillo-Rangel,Sylvia Elena Totsuka-Sutto,Araceli Castillo-Romero

doi:10.1155/2019/1302985

Abstract

The therapeutic effects of telmisartan, an angiotensin II receptor antagonist and a peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist, have been demonstrated in several disorders. It has antioxidant and immune response modulator properties and has shown promising results in the treatment of an ischemia/reperfusion (I/R) lesion. In this study, a skeletal muscle (right gastrocnemius muscle) I/R lesion was induced in rats and different reperfusion times (1 h, 24 h, 72 h, 7-day, and 14-day subgroups) were assessed. Furthermore, levels of oxidative markers such as enzymatic scavengers (catalase (CAT) and superoxide dismutase (SOD)) and metabolites (nitrates and 8-oxo-deoxyguanosine) were determined. The degree of tissue injury (total lesioned fibers and inflammatory cell count) was also evaluated. We observed an increase in CAT and SOD expression levels under telmisartan treatment, with a decrease in injury and oxidative biomarker levels in the 72 h, 7-day, and 14-day subgroups. Telmisartan reduced oxidative stress and decreased the damage of the I/R lesion.

Highlights

Ischemia reperfusion (I/R) is a phenomenon that occurs after the occlusion of arterial blood flow to a specific organ or tissue
We evaluated the histological impact of telmisartan on I/R lesion-induced muscle tissue damage in the limbs of Wistar rats
We found that telmisartan produced changes in the superoxide dismutase (SOD)-2 and CAT gene expression but to a different degree and time-course regarding reperfusion

Summary

Introduction

Ischemia reperfusion (I/R) is a phenomenon that occurs after the occlusion of arterial blood flow to a specific organ or tissue. It is related to an exacerbation of the initial lesion and followed by several physiopathological mechanisms in the affected cells, such as increments of cations in cytosol, formation of reactive oxygen species and nitrogen species, disruption of the signaling redox (oxidative stress (OS)), mitochondrial lesion, transcriptional reprograming, endothelial lesion, no-reflow phenomenon, immunitymediated lesion, apoptosis, autophagy, and necrosis From all these processes, the pathological changes in the affected tissue can be divided into acute (first 72 h) and chronic (15–90 days) at onset, which are determined by factors, such as the time of ischemia and the response to inflammation and oxidative stress [3, 4].

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