Protective effects of irigenin against 1-methyl-4-phenylpyridinium-induced neurotoxicity through regulating the Keap1/Nrf2 pathway

The rhizome of Belamcanda chinensis possesses antiinflammatory and antioxidant activities. However, the effect of irigenin, isolated from the rhizome of B. chinensis, on 1-methyl-4-phenylpyridinium (MPP+)-induced neurotoxicity is unknown. MTT assay showed that MPP+ exposure dose dependently inhibited the viability of mouse microglia BV-2 cells, whereas irigenin suppressed MPP+-induced viability reduction. The production of nitric oxide, prostaglandin E2, tumor necrosis factor-alpha and interleukin-6 were increased by MPP+ treatment, which were abolished by irigenin treatment. Irigenin-attenuated MPP+-induced increase of malondialdehyde content and activities of superoxide dismutase, catalase and glutathione peroxidase in BV-2 cells. Irigenin treatment also repressed apoptosis, caspase-3/7 activity and Cytochrome C expression in MPP+-challenged BV-2 cells. Interestingly, irigenin activated the Keap1/Nrf2 pathway in MPP+-induced BV-2 cells. Nrf2 knockdown attenuated the effects of irigenin on MPP+-induced viability reduction, inflammation, oxidative stress and apoptosis in BV-2 cells. In conclusion, irigenin alleviated MPP+-induced neurotoxicity in BV-2 cells through regulating the Keap1/Nrf2 pathway.

Automated summary

Iridencin alleviated MPP+-induced neurotoxicity in BV-2 cells by regulating the Keap1/Nrf2 pathway, suppressing inflammation and oxidative stress.