Protective Effects of Cinnamaldehyde on the Oxidative Stress, Inflammatory Response, and Apoptosis in the Hepatocytes of Salmonella Gallinarum-Challenged Young Chicks

Figure 10

Summary of events of S. gallinarum infection to chicken hepatocytes and protective effects of cinnamaldehyde. S. gallinarum infection to chicken hepatocytes disrupts the electron transport chain resulting in high ROS production, decrease in Ψm, and cytochrome c release from mitochondria. Cytochrome c triggers caspase-3 activity, which eventually causes apoptosis. Bacterial effectors result in increased glycolysis and ATP production. At the same time, increased hepatic CFU, MyD88/NF-κB dependent inflammatory response, serum AST, and ALT levels were also found in S. gallinarum-infected chicken hepatocytes. In contrast, cinnamaldehyde treatment resulted in decreased ROS production and relatively normal mitochondrial membrane potential, and cytochrome c release was significantly lower than that of the infected group. Moreover, caspase-3 activity and extent of apoptosis were also significantly lower than that of the challenge group. Similarly, cinnamaldehyde protects the host from metabolic changes, indicated by significantly lower ATP concentration in the treatment group than that of the challenge group. Lower ALT and AST levels, inflammatory response, H&E changes, TEM changes, and hepatic CFU were also observed in the treatment group.