CTRP3/AMPK pathway plays a key role in the anti-hypertrophic effects of cyanidin-3-O-glucoside by inhibiting the inflammatory response.

BACKGROUND

Cardiac hypertrophy can be a pathological process that impairs heart function. Anthocyanins are a well-characterized type of natural antioxidant, and recent studies have shown that this type of compound has potential cardioprotective effects against different disorders, such as cardiac hypertrophy.

OBJECTIVES

We assessed the anti-hypertrophy potential of cyanidin-3-O-glucoside (C3G) and the mechanism associated with any observed effects.

MATERIAL AND METHODS

Hypertrophy symptoms were induced using the transverse aortic constriction (TAC) operation in vivo and angiotensin II (Ang II) in vitro. The effect of C3G on the development of hypertrophic symptoms was then determined. Moreover, we examined the influence of CTRP3 inhibition on the anti-hypertrophy function of C3G.

RESULTS

The TAC operation induced cardiac fibrosis and heart weight increase, which was associated with increased production of cytokines and suppressed activity of the CTRP3/AMPK pathway. The impairments of heart structure and function were attenuated by C3G. Angiotensin II induced size increases of neonatal rat cardiomyocytes (NRCMs) in vitro, and this effect was inhibited by C3G. Furthermore, the inhibition of CTRP3 counteracted the function of C3G by promoting NRCM hyperplasia and inflammation.

CONCLUSIONS

The results of the current study showed that the activation of CTRP3 contributed to the anti-hypertrophy effects of C3G.