Lycopene regulates the formation of calcium oxalate kidney stones by modulating reactive oxygen species(ROS) and NF-κB pathways.

This study aims to determine whether lycopene can reduce oxi-dative stress and inflammatory damage in HK-2 cell cultures induced by cal-cium oxalate crystallization through the modulation of reactive oxygen species (ROS) and the NF-κB signalling pathway. Cell cultures were divided into four groups: The control group, the Model group (COM + oxalic acid), and two Lyco-pene intervention groups (COM + oxalic acid + 5/10 μmol/L lycopene). After 24 hours of culture, viability, LDH, oxidative and anti-oxidative parameters, mi-tochondrial membrane potential, MCP-1, IL -6, apoptosis and related proteins, and activation and expression of NF-κB were determined by adequate methods. When compared to the control group, the model group exhibited decreased cell activity (p<0.001) and GSH and SOD antioxidant capacity (p<0.05), along-side a significant rise in LDH, MDA, and the release of inflammatory mediators MCP-1 and IL -6 (p<0.05). The levels of protein expression for NF-κB, OPN, Bax, Cyt C, and active Caspase-3 were increased (p<0.05), whereas Bcl-2 protein expression significantly diminished (p<0.05). The mitochondrial membrane potential decreased. Lycopene intervention reduced the damage to HK-2 cells (p<0.05), accompanied by decreased levels of LDH, MDA, and inflammatory factors MCP-1 and IL -6 (p<0.05), and increased GSH and SOD antioxidant capacity (p<0.05). The mitochondrial membrane potential was observed to in-crease. No significant changes were observed in the expression of NF-κB. The expressions of OPN, Bax, Cyt C, and Caspase-3 decreased (p<0.05), whereas the level of Bcl-2 protein expression increased. In conclusion, lycopene decreas-es cellular damage by inhibiting lipid peroxidation induced by calcium oxa-late crystals and oxalate, enhancing intracellular antioxidant enzyme activity, modulating ROS and NF-κB inflammatory pathways, improving mitochondrial integrity, and exerting anti-inflammatory effects through the inhibition of the mitochondrial-mediated Bax/Caspase-3 signalling pathway.