Pyrroloquinoline quinone attenuates isoproterenol hydrochloride‑induced cardiac hypertrophy in AC16 cells by inhibiting the NF‑κB signaling pathway.

Pyrroloquinoline quinone (PQQ) is a naturally occurring redox co‑factor that functions as an essential nutrient and antioxidant, and has been reported to exert potent anti‑inflammatory 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 anti‑inflammatory effects of PQQ were investigated in Iso‑treated 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 hypertrophy‑associated proteins. The results revealed that pre‑treatment with PQQ significantly inhibited the expression of cardiac hypertrophy marker proteins, such as atrial natriuretic peptide, brain natriuretic peptide and β‑myosin heavy chain. PQQ also inhibited the activation of the nuclear factor (NF)‑κB signaling pathway in Iso‑treated AC16 cells, thus inhibiting the nuclear translocation of NF‑κB 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.