Objective: Made LLC-PK1 damage model induced by high glucose and observing the protection effect and its mechanisms of LLC-PK1 injury induced by high glucose.
Methods: The proliferation of LLC-PK1 induced by high glucose was tested by CCK-8 and the apoptosis rat and the contents of reactive oxygen species (ROS) of LLC-PK1 damaged by high glucose was observed by flow cytometry after administration of different concentration alpha-linolenic acid (ALA).
Result: High glucose could obviously inhibit the proliferation of LLC-PK1 The apoptotic rates of LLC-PK1 intervened by ALA (50-100 micromol/L) in the preconditioning group and the persistent intervention group were lower than those in the positive control group (P < 0.05). The contents of ROS of LLC-PK1 in the persistent intervention group were lower than those in the positive control group when the concentration of ALA were from 10 micromol/L to 100 micromol/L (P < 0.05, P < 0.01). The contents of ROS of LLC-PK1 in the preconditioning group were lower than those in the positive control group when the concentration of ALA was 50 micromol/L (P < 0.05).
Conclusion: The model of LLC-PK1 induced by high glucose provided fine chances for the intervention of renal tubular epithelial cells in DN. ALA were expected to be a protectant to prevent high glucose damage of renal tubulars. Decreasing the active oxygen generation may be one of the mechanism of the protective effects on LLC-PK1 by ALA.