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 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 betamyosin heavy chain. PQQ also inhibited the activation of the nuclear factor (NF)kappaB signaling pathway in Isotreated AC16 cells, thus inhibiting the nuclear translocation of NFkappaB 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.