A nonenzymatic electrochemical sensor for the detection of hydrogen peroxide in vitro and in vivo fibrosis models

Fibrosis occurs due to the excessive deposition of extracellular matrix caused by cell injury. After various types of tissue injury, the dysregulation of the internal response can eventually lead to the destruction of organ structure and dysfunction. There is increasing evidence that oxidative stress, which is characterized by excessive production of hydrogen peroxide (H2O2), is an important cause of fibrosis. Therefore, we synthesized a biosensitive and efficient electrochemical H2O2 sensor based on PtNi nanoparticle-doped N-reduced graphene oxide (PtNi-N-rGO) to detect H2O2 released from transforming growth factor β1 (TGFβ1)-induced myofibroblast. In addition, the sensor could easily detect changes in H2O2 in the lung and bronchoalveolar lavage fluid (BALF) of mice with pulmonary fibrosis. Furthermore, the sensor could also detect H2O2 in activated hepatic stellate cells and the liver of carbon tetrachloride (CCl4)-induced liver fibrosis. Moreover, the alterations in H2O2 detected by the sensor were consistent with nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) protein expression and the staining results of pathological sections. Taken together, these results highlight the use of H2O2 sensors for the rapid detection of fibrosis and facilitate the rapid evaluation of antifibrotic drug candidates.