Pyrroloquinoline quinone attenuates isoproterenol hydrochloride­induced cardiac hypertrophy in AC16 cells by inhibiting the NF­κB signaling pathway.

ABSTRACT

Pyrroloquinoline quinone (PQQ) is a naturally occurring redox co­factor that functions as an essential nutrient and antioxidant, and has been reported to exert potent anti­inflammatory effects. However, the therapeutic potential of PQQ for isoproterenol hydrochloride (Iso)­induced cardiac hypertrophy has not yet been explored, at least to the best of our knowledge. In the present study, the anti­inflammatory effects of PQQ were investigated in Iso­treated AC16 cells, a myocardial injury cellular model characterized by an increase in the apparent surface area of the cells and the activation of intracellular cardiac hypertrophy­associated proteins. The results revealed that pre­treatment with PQQ significantly inhibited the expression of cardiac hypertrophy marker proteins, such as atrial natriuretic peptide, brain natriuretic peptide and ß­myosin heavy chain. PQQ also inhibited the activation of the nuclear factor (NF)­κB signaling pathway in Iso­treated AC16 cells, thus inhibiting the nuclear translocation of NF­κB and reducing the phosphorylation levels of p65. On the whole, the findings of this study suggest that PQQ may be a promising therapeutic agent for effectively reversing the progression of cardiac hypertrophy.