Tranilast treatment attenuates cerebral ischemia‐reperfusion injury in rats through the inhibition of inflammatory responses mediated by NF‐ κB and PPARs

Abstract

Ischemia‐reperfusion injury (IRI) occurs when blood supply returns to tissue after interruption, which is associated with life‐threatening inflammatory response. Tranilast is a widely used anti‐allergic agent in the treatment against bronchial asthma and keloid. To study the function of tranilast, we used IRI rat model. The brain tissues of IRI rats with or without tranilast treatment were collected. Neuronal apoptosis in the brain was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling assay, and pro‐inflammatory cytokine levels were measured by qRT‐PCR and enzyme‐linked immunosorbent assay. The expression levels of nuclear factor‐κB (NF‐κB), inhibitor of κB (IκB) and peroxisome proliferator‐activated receptors (PPARs) were detected by Western blot. The results showed that tranilast treatment reduced neuronal apoptosis in the brain of IRI rats. Tranilast enhanced the short term and long term memory to novel object recognition paradigm. Tranilast treatment decreased the mRNA and protein levels of multiple pro‐inflammatory cytokines, and affected NF‐κB and IκB protein expressions. Tranilast promoted the expressions of PPAR‐α and PPAR‐γ. Our findings demonstrate that tranilast treatment could attenuate cerebral IRI by regulating the inflammatory cytokine production and PPAR expression. Tranilast is a potential drug for IRI treatment in clinic.

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