Apigenin attenuates acrylonitrile-induced neuro-inflammation in rats: Involved of inactivation of the TLR4/NF-κB signaling pathway



• Apigenin protected the brains from acrylonitrile-induced neurotoxicity.
• Apigenin inhibited neuro-inflammation via downregulating the TLR4/NF-κB signaling pathway.
• Apigenin suppressed neuronal apoptosis expressed as inhibiting mitochondria-mediated apoptosis pathway.



Acrylonitrile (ACN) is often found in the productions of synthetic fibers, rubber, and plastics. Exposure to ACN could cause pathological changes of the nervous system, which appeared early and were very serious. Current studies have found that the neurotoxicity is mainly related to oxidative damage and inflammation induced by ACN. Apigenin (AP) is a flavonoid subtype compound that is less toxic, non-mutagenic, and widely distributed in many types of vegetables and fruits. Studies have confirmed that it has nice antioxidant, anti-inflammatory and anti-apoptotic properties in the nervous system and related disease models, such as Alzheimer's disease. In this study, we used AP (117, 234 and 351 mg·kg1) pretreatment intragastrically to resist the neurotoxicity caused by ACN gavage (46 mg·kg−1) for 28 days, and then detected the oxidative stress, inflammation mediated by the TLR4/NF-κB signaling pathway, and apoptosis to evaluate the protective effect of AP. The results showed that AP could lessen the autonomic activities of rats, and improve the abnormal morphology of neurons induced by ACN. AP could also reduce the oxidative stress, downregulate the TLR4/NF-κB signaling pathway, decrease the levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), and inhibit the mitochondria-mediated neuron apoptosis. Immunofluorescence result showed that AP could decrease the activation and nuclear transfer of NF-κB induced by ACN. These results suggested that AP could protect the brain against ACN-induced neurotoxicity by inhibiting the TLR4/NF-κB signaling pathway and could exhibit a neuroprotective effect.


Link to the publication : https://www.sciencedirect.com/science/article/pii/S1567576919304680