The Antioxidant and Anti-Inflammatory Effects of the Main Carotenoids from Tomatoes via Nrf2 and NF-κB Signaling Pathways

Oxidative stress and inflammation are crucial factors in the development of cardiovascular diseases. In previous research, the oxidative stress and inflammation models have frequently been explored independently. In the current study, we investigated the antioxidant and anti-inflammatory effects of tomato extract and its two main carotenoids (lutein and lycopene) with various concentrations using a rat cardiomyocyte model of co-existing oxidative stress and persistent chronic inflammation. It was discovered that the antioxidant effects of 0.5-5 mu M lutein, 0.5-5 mu M lycopene, and 50-200 mu g/mL tomato extract increased in a dose-dependent manner. However, the pro-oxidation effects emerged by measuring the antioxidant-related indices, including the levels of ROS, SOD, and GPX in H9c2 cells as concentrations exceeded those mentioned above. The anti-inflammatory effects of lutein, lycopene, and tomato extract were simultaneously strengthened with higher concentrations, potentially due to the suppression of the NF-kappa B signaling pathway. Furthermore, high concentrations of lutein, lycopene, and tomato extract potentially regulated Nrf2/HO-1 and NF-kappa B signaling pathways dependent on TGF-1 beta and IL-10 to demonstrate high concentrations of pro-oxidation and anti-inflammation effects. Our findings indicate that the dose-effect regulatory mechanisms of antioxidant and anti-inflammatory properties among lutein, lycopene, and tomato extract will be advantageous in developing more effective therapeutic strategies to prevent cardiovascular diseases.

Automated summary

The study investigated the antioxidant and anti-inflammatory effects of tomato extract and its carotenoids lutein and lycopene. It was found that these compounds exhibited dose-dependent antioxidant effects but showed pro-oxidation effects at higher concentrations. The anti-inflammatory effects were enhanced at high concentrations and potentially mediated through the inhibition of the NF-kappa B signaling pathway.