Rutaecarpine ameliorates cardiomyocyte injury induced by high glucose by promoting TRPV1-mediated autophagy.

AIM: Diabetic cardiomyopathy (DCM) is a dominant factor contributing to diabetic death. Rutaecarpine has many cardiovascular biological effects and anti-high-glucose activity. Therefore, this paper aimed to investigate the impact of rutaecarpine on high glucose (HG)-elicited cardiomyocyte injury.

METHOD: Cell counting kit 8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU), TdT-mediated dUTP Nick-End Labeling (TUNEL) assays judged H9c2 cell activity and apoptosis, and oxidative stress was assessed by corresponding assay kits. The expression of apoptosis, oxidative stress, autophagy-associated factors and TRPV1 were examined with western blot. IF assay tested GFP-LC3 expression.

RESULTS

As a result, rutaecarpine had no obvious effect on the viability of H9c2 cells while elevated HG-exposed H9c2 cell viability. Rutaecarpine inhibited the apoptosis and oxidative stress of H9c2 cells induced by HG. In addition, rutaecarpine activated TRPV1 to induce autophagy. However, inhibition of TRPV1 inactivated the autophagy, which drove HG-evoked H9c2 apoptosis and oxidative stress.

CONCLUSIONS

In conclusion, rutaecarpine suppressed HG-stimulated H9c2 cell viability injury, apoptosis as well as oxidative stress via promoting TRPV1-mediated autophagy (Fig. 10, Ref. 40).