Matrine suppresses AGE-induced HAEC injury by inhibiting ROS-mediated NRLP3 inflammasome activation.

Diabetes is characterized by a high level of advanced glycation end products (AGEs), which induce damage in the arterial endothelium. Matrine has been shown to have cardioprotective effects. This study's aim was to investigate the protective effects and possible molecular mechanisms of matrine in AGE-induced human aortic endothelial cell (HAEC) injury. Cultured HAECs were treated with AGEs and/or serially diluted matrine. Cell viability was evaluated by MTT assay. Intracellular reactive oxygen species production was determined by flow cytometry. The expression levels of nucleotide-binding, leucine-rich repeat, and pyrin-domain-containing 3 (NLRP3), adaptor molecule apoptosis-associated speck-like protein, cleaved caspase-1 and interleukin-1β (IL-1β) were assessed by Western blotting; the concentration of IL-1β in culture supernatants was determined by enzyme-linked immunosorbent assay (ELISA). In a concentration-dependent manner, matrine co-treatment with AGEs substantially inhibited the reduction in cell viability and the increase in intracellular reactive oxygen species induced by AGEs. Co-treatment with matrine significantly inhibited the AGE-induced increase in NLRP3, ASC, caspase-1, p20 and IL-1β expression in HAECs in a concentration-dependent manner. Moreover, the AGE-mediated increase in IL-1β expression in cell culture supernatants was also reduced by co-treatment with matrine in a concentration-dependent manner. AGEs induced HAEC injury by inducing reactive oxygen species -mediated NLRP3 inflammasome activation. Matrine recovered HAEC viability by inhibiting reactive oxygen species -mediated NLRP3 inflammasome activation.