Abstract

The neuroprotective effects of catalpol had been well demonstrated in many studies. Nevertheless, little work was done to investigate the cardioprotective effects of catalpol. This study was designed to explore whether catalpol protected myocardium against isoproterenol (ISO)-induced myocardial injury through attenuating oxidative stress and suppressing inflammation. Histopathological changes were assessed by hematoxylin and eosin staining. Results show that catalpol could effectively suppress the histopathological changes including myocardial structure damage and leucocyte infiltration. Oxidative stress and antioxidant status were also analysed. Results show that catalpol could significantly attenuate the increase of myocardial malondialdehyde (MDA) and renew the activities of superoxide dismutase (SOD). Furthermore, the results of real time reverse transcription polymerase chain reaction (RT-PCR) and Western-blot analysis showed that catalpol could inhibit the upregulation of the expressions of tumor necrosis factor-a (TNF-a) and interleukin-1β (IL-1β) caused by ISO. In conclusion, our data suggest that catalpol had a protective effect against ISO-induced cardiotoxicity in rat, by maintaining endogenous antioxidant enzyme activities and alleviating inflammatory response. This study provides novel insights that catalpol treatment could be an approach for the prevention of ischemic heart disease.

Key words: Catalpol, isoproterenol, inflammation, oxidative stress, myocardial injury.

Abbreviation

ISO, Isoproterenol; RT-PCR, reverse transcription polymerase chain reaction; TNF-a, tumor necrosis factor-a; IL-1β, interleukin-1β; MDA, malondialdehyde; SOD, superoxide dismutase.