Ephedrine causes liver toxicity in SD rats via oxidative stress and inflammatory responses.

Abstract

Ephedrine abuse has spread in many parts of the world and severely threatens human health. The mechanism of ephedrine-induced toxicity still remains unclear. This study was performed to investigate the effects of ephedrine treatment on the liver and explore the underlying mechanisms. Sprague Dawley rats were divided into saline and ephedrine groups. Rats were treated with ephedrine at 20 mg/kg or 40 mg/kg (n = 10) by oral gavage daily for 7 days. Pathological changes were examined by hematoxylin and eosin staining and terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling assay. Enzyme-linked immunosorbent assays were used to measure the liver functional markers, oxidative stress markers, and inflammatory cytokines. Real-time polymerase chain reaction and Western blot were used to measure gene and protein expression, respectively. Our data showed that ephedrine treatment increased hepatocellular cell apoptosis and impaired liver function. Moreover, ephedrine treatment increased oxidative stress and inflammatory responses, which may be due to the increase of transforming growth factor β (TGF-β)/Smad3 expression. Our study demonstrated that short-term treatment of ephedrine caused liver toxicity in rats through regulating TGF-β/Smad pathway.