NADPH Oxidase Hyperactivity Contributes to Cardiac Dysfunction and Apoptosis in Rats with Severe Experimental Pancreatitis through ROS-Mediated MAPK Signaling Pathway

Figure 10

Possible mechanisms responsible for the effect of Nox on SAP-associated cardiac injury. During pancreatitis, a large number of proinflammatory cytokines and toxic substances are released into bloodstream, which can exert stimulation to Nox in the myocardial cell. The hyperactivity of Nox results in the overproduction of ROS and activates the redox-sensitive MAPK signaling pathways. These events upregulate the expression of caspase-associated proteins, which ultimately induces cell apoptosis. Pretreatment with apocynin to inhibit the activity of Nox can lead to the decrease in ROS production under SAP conditions, thus alleviating the activation of downstream signaling pathways and thereby affording beneficial effects.