Tropisetron inhibits high glucose-induced calcineurin/NFAT hypertrophic pathway in H9c2 myocardial cells.

Objectives: Cardiomyocyte hypertrophy is an important structural feature of diabetic cardiomyopathy. Calcineurin/nuclear factor of activated T-cell (NFAT) pathway plays a central role in the pathogenesis of cardiac hypertrophy. The purpose of this study was to investigate the effects of tropisetron, a novel calcineurin inhibitor, on high glucose (HG)-induced cardiomyocyte hypertrophy and its underlying mechanism.

Tropisetron ameliorates early diabetic nephropathy in streptozotocin-induced diabetic rats.

It has been well established that oxidative stress and inflammation are involved in the pathogenesis of diabetic nephropathy. It has been shown that tropisetron exerts anti-inflammatory and immunomodulatory properties. The current study was designed to investigate protective effects of tropisetron on early diabetic nephropathy in streptozotocin-induced diabetic rats.

The cardioprotective effects of an antiemetic drug, tropisetron, on cardiomyopathy related to doxorubicin.

Cardiotoxicity is a life-threatening side effect of doxorubicin (DOX). Although the responsible mechanisms are largely unknown, it is demonstrated that DOX induces an elevation in the level of creatine kinase isoenzyme, lactic dehydrogenase, creatine phosphokinase, and troponin T in serum and reduces body/heart weight. In addition, cardiotoxicity is further confirmed by changes in ECG parameters and papillary muscle contractile force.