Besides its anti-inflammatory effect, PQQ exerts anti-neuroinflammatory effects on microglial cells. It also has an antioxidant property. These properties are related to its ability to antagonize several types of oxidative stress-induced cell damage. Especially, PQQ is effective in neutralizing superoxide radicals. In addition, it inhibits thioredoxin reductase 1. In a previous study, PQQ reduced the production of lipid peroxidation and attenuated the synthesis of amyloid proteins associated with Alzheimer’s disease.

During the first stage of heart failure development, cardiac hypertrophy occurs. The increase in the number of cardiomyocytes results in a decrease in their capacity to regenerate lost tissue. This process is commonly referred to as the compensatory period of cardiac hypertrophy.

In order to investigate the possible protective effect of PQQ against Iso-induced cardiac hypertrophy, Iso-treated AC16 cells were treated with a PQQ concentration of varying concentrations. In each of the groups, cells were seeded into a 96-well plate at a density of 5×103 cells/well. The cell viability was determined by using the CCK-8 assay kit.

The cells were then incubated with H2O2 in DMEM without FBS for 1 h. In addition, cell proliferation and metabolic activity were measured. The results showed that Iso-treated cells increased NF-kB translocation to the nucleus and hypertrophic markers, whereas those in the pre-treated group were decreased. In the Iso-treated group, the expression of ANP protein was significantly increased.

Inhibition of NF-kB phosphorylation by PQQ is another mechanism of the protective effect of PQQ against Iso-induced hypertrophy. In addition, PQQ has been reported to enhance the mitochondrial fission and fusion process.